Stroke is defined as a clinical syndrome consisting of rapidly developing clinical signs of focal (or global in case of coma) disturbance of cerebral function lasting more than 24 h or leading to death with no apparent cause other than a vascular origin [4]. Keeping this definition in mind is helpful when reviewing a suspected stroke patient, especially as a history of acute onset focal deficit, is characteristic of stroke. Important from history-taking and examination is to establish if any relevant trauma has occurred that may have contributed to a large vessel dissection or intracerebral haemorrhage (e.g. head or neck injury) or become relevant as a contraindication to specific therapy (e.g. occult fracture). Furthermore, a drug history, especially relating to anticoagulation, antiplatelets or drugs of abuse, is important to obtain and, if necessary, obtain pharmacy records or examine patient’s personal belongings. Additionally, information regarding vascular risk factor should be obtained. Identifying if the patient has vomited or is suspected of aspirating is also imperative.

Coma is a rare initial feature in posterior circulation stroke (2 % in one registry study), but it is important to distinguish coma as a result of basilar thrombosis [5]. Useful methods of identifying basilar artery occlusion as a cause of coma include a history suggestive of preceding posterior circulation TIA episodes and sudden onset of coma [6]. Clinical examination findings in posterior circulation stroke may include eye movement abnormalities, focal lateralising signs and pupil abnormalities [6–8]. The predominant features of pontine infarction and/or basilar artery occlusive disease are motor and oculomotor [6–8].

Neurological examination may have to be adapted, and specific factors such as presence of endotracheal tube or sedation in ICU patients should be taken into account. Measuring the level of consciousness and establishing if patient is conscious is imperative, and helpful if measured sequentially in a standardised manner. The National Institute of Health Stroke Score (NIHSS) is a standardised clinical scale used in acute stroke. It is scored from 0 (no deficit) to a maximum score of 42, and includes assessment of the level of consciousness, language, eye movements, visual fields, sensation, sensory extinction inattention, facial and limb weakness, and dysarthria and ataxia [9]. In intubated patients, however, certain components, for example, dysarthria cannot be elicited, and this should be noted.

The majority of stroke patients are managed at the ward or specialist ward (e.g. stroke unit) level. Admission to dedicated stroke units is associated with improved functional outcome [10–12].

However, some patients require admission to ICU for a number of reasons (see Table 3.1), the commonest of those being for mechanical ventilation and/or invasive haemodynamic and neurological monitoring.

Prognostication is important for assessing whether or not to admit to ICU [14]. This should rely on clinical and radiological assessment, with particular emphasis on premorbid function when discussing with relatives. Clear and constructive lines of communication between families, stroke physicians and intensivists are vital.

When assessing a critically ill patient, many tasks happen simultaneously (e.g. treating an immediate life-threatening problem, assessing airway, breathing and circulation, general clinical examination and focused history-taking from the patient or a proxy such as relatives, medical, paramedical or nursing staff). However, we have described them in a systemic manner here for ease of understanding.

A number of clinical scenarios can result in airway concerns. Posterior circulation strokes and more particularly those patients with brain stem involvement may have reduced levels of consciousness and be unable to protect their own airway [5–8]. Similarly, those with a degree of cerebral oedema surrounding a large infarct or haemorrhage may have elevated intracranial pressure leading to brain herniation and coma.

It is generally accepted that those with a GCS ≤ 8 are unable to protect their own airway and require endotracheal intubation. Other concerns which may favour securing the airway would include hypoxaemia. However, a larger concern would likely be control of ventilation, and the avoidance of hypercarbia and its deleterious effects on intracranial pressure.

Stroke patients may require supplemental oxygen therapy due to aspiration, hypoventilation or both. The percentage of haemoglobin saturated with oxygen remains the greatest variable when describing oxygen delivery to tissues. This has particular relevance when referring to the ischaemic penumbra around an area of ischaemia.

Hypoxaemia is common following stroke and adversely effects outcome. Causes of hypoxaemia following stroke can include aspiration, respiratory tract infection, acute respiratory distress syndrome, pulmonary embolism, pulmonary oedema (neurogenic or cardiogenic) and dysfunction of centrally regulated ventilation.

However, there is some controversy regarding the routine administration of supplemental oxygen which may be detrimental, irrespective of stroke severity [3].

As mentioned above, control of ventilation and specifically CO₂ levels and their consequent effects on cerebral blood flow are of importance, particularly when there is a concern regarding raised intracranial pressure from, for example, an intracranial haematoma, peri-ischaemic oedema or a posterior fossa lesion, where the tentorium cerebelli restricts expansion of oedematous tissue, thereby risking herniation of the brain stem through the foramen magnum.

The rationale for treatment of severe hypertension is to lower the risk of haemorrhagic transformation of an ischaemic area (typically large), however aggressive blood pressure reductions may adversely affect cerebral perfusion, especially in the penumbra, thus exacerbating ischaemic damage [3].

Blood pressure should be controlled to ≤185/110 mmHg in patients who may be appropriate for thrombolysis and treatment given to patients who are not thrombolytic candidates whose blood pressure is >220 mmHg systolic or >120 mmHg diastolic on repeated measurements or whose mean arterial pressure exceeds 130 mmHg [12, 15].

Autoregulation is a physiological process which refers to the capacity of cerebral circulation to adjust its resistance to maintain a constant cerebral blood flow regardless of changing systemic blood pressure or cerebral perfusion pressure [16]. An increase in mean arterial pressure (MAP) increases the transmural vessel tension causing an increase in vascular smooth muscle tone (with the converse also the case). It occurs between MAP of 50–150 mmHg, is a very rapid process, and is mediated primarily by endothelium-derived relaxing factor and nitric oxide (EDRF/NO) [17].

Outside these parameters, cerebral blood flow becomes pressure-dependent and directly changes with changes in MAP. In chronic arterial hypertension, the upper and lower limits of autoregulation are both displaced to higher levels, shifting the curve to the right. In hypertensive patients, cerebral hypoperfusion occurs at higher values of MAP, compared with healthy individuals. The limits of autoregulation are affected by various factors, including sympathetic nerve activity, PaCO₂ and pharmacological agents. In particular, cerebral autoregulation may be impaired after any brain injury, for example, ischaemic stroke, intracranial haemorrhage or ruptured aneurysm.

A particular note should be paid to the presence of hypertension with bradycardia (Cushing’s response), which is associated with severe intracranial hypertension and impending coning.

Systemic examination should include a check for evidence of significant BP arm differences, as stroke may be the presenting feature of acute aortic dissection.

A patient’s level of consciousness may be assessed by a number of different methods. The ‘AVPU’ scale describes a motor, verbal or eye-opening response to differing methods of stimuli (Alert/Voice/Pain/Unresponsive). It is essentially a modified assessment of Glasgow Coma Scale (GCS, Table 3.2) [13]. GCS assessment itself may also be used, albeit outside of the context of head trauma for which it was initially designed. However, most clinicians have an understanding of the various components of GCS, and its use in stroke is therefore not unreasonable while acknowledging the limitations of its use in that context.

Eye movement and detecting if eye movement on command can be performed is an important clinical sign to elicit in establishing the level of consciousness, especially in patients who may have brain stem ischaemia.

Table 3.3 lists common and/or useful neurological signs associated with stroke, and Table 3.4 describes the classic stroke syndromes classified by anatomical clinical syndrome and/or vascular territory involved.

General examination of a patient and environmental assessment is an integral part of assessment (e.g. of wallet pockets of clothes) for regular medication etc.

Inspection for rash, for example, as in zoster vasculopathy (as may be seen with chicken pox or shingles), orvasculitis is also important, as it may highlight a potentially treatable cause of stroke [18].

Additionally, it is important to look for evidences of bruising, which may indicate undisclosed trauma or perianal trauma in the case of ‘body packing’ of substances such as cocaine. Examination for stigmata of endocarditis or murmurs is worth performing at initial assessment.

In the hyperacute phase, blood glucose should be checked as a priority, as hypoglycaemia and hyperglycaemia may mimic stroke syndromes.

In the acute phase, brain imaging urgently with either CT brain or MRI brain is required in suspected stroke to distinguish haemorrhage from ischaemic stroke. CT imaging is fast and usually accessible. In the acute phase, CT imaging with CTA vessel imaging may allow identification of large vessel occlusion or dissection. In many centres, CT and CTA are more readily available in the acute phase, than MRI, and are helpful if MRI is contraindicated. MRI compatibility of devices and monitoring equipment is an additional challenge in ICU patients. MRI brain with diffusion-weighted imaging (DWI) is far more sensitive than CT brain, especially for brain stem ischaemia, although false-negative can occur with early DWI imaging [19, 20]. MRI/MRA with dedicated fat saturation sequences is especially helpful for identifying dissection. MRI can help verify vascular territory (Figs. 3.1 and 3.2).

12-lead ECG should be performed to look for evidence of ischaemia or arrhythmia [12].

Blood gas analysis in the hyperacute setting may provide important measure of haemostasis.

Thrombolysis with alteplase is indicated in ischaemic stroke when eligibility criteria are met. Trial data from originally the NINDS trial and the more recent ECASS3 trial provide the basis for licensing of alteplase in acute ischaemic stroke [15, 24]. The open label IST3 trial further supports it use [25]. Registry data from the SITS registry supports its use beyond the setting of clinical trial populations, including in patients over 80 years of age who match the other eligibility criteria [26]. Some controversy exists regarding the strength of the trial data and the effectiveness of the treatment, but appropriate patient selection is pivotal in considering the effectiveness of therapy [27]. Practical difficulties in decision-making regarding thrombolysis include poorly controlled glucose levels, difficult to control BP, significant pre-existing cerebrovascular disease, unclear onset time or concern that a minor deficit may have preceded a more recent deterioration, as well as availability of trained staff and adherence to protocols and guidelines. Although every minute counts in terms of neurons lost, the decision to thrombolyse a patient needs to be made judiciously. Adverse effects of thrombolysis include bleeding risk and allergic reaction. It is important to check blood results when available, e.g. platelets and INR, because although the initial bolus of thrombolytic agent may be given before results of investigations are available, the relevant parameters should be checked before the infusion is given.

Contraindications to tPA based on its license for use include any intracerebral haemorrhage, known or suspected CNS lesion with high likelihood of haemorrhage after tPA (e.g. brain tumour, abscess, vascular malformation, aneurysm, contusion, endocarditis), clinical presentation suggestive of subarachnoid haemorrhage even with normal CT, uncontrolled hypertension (SBP > 180 or DBP > 110 at time of tPA to begin), history of intracranial haemorrhage, active internal bleeding, fracture or acute trauma, stroke, serious head trauma, intracranial or intraspinal surgery within 3 months or bleeding disorder [15, 24].Recent studies have looked at mechanical treatments include the use of catheters to directly deliver (during angiography) a clot-disrupting or retrieval device to a thromboembolus that is occluding a cerebral artery. Mechanical thrombectomy, in addition to intravenous thrombolysis within 4.5 hours when eligible, is recommended to treat acute stroke patients with large artery occlusions in the anterior circulation up to 6 hours after symptom onset. Mechanical thrombectomy should not prevent the initiation of intravenous thrombolysis where this is indicated, and intravenous thrombolysis should not delay mechanical thrombectomy which should be performed as soon as possible after its indication.

Six studies have reported positive results with modern mechanical approaches to re-perfusion. The number needed to treat to achieve one additional patient with independent functional outcome was in the range of 3·2-7·1 and, in most patients, was in addition to the substantial efficacy of intravenous alteplase [28]. Thrombolysis therapy, despite the low numbers needed to treat to have benefit, will ever only be suited to a fraction of patients who have an ischaemic stroke, especially if there are delays in patients accessing appropriate care [29].