The characteristics of this period are markedly different depending on the clinical grade of the aSAH. Patients with aSAH of good clinical grade (World Federation of Neurosurgical Societies (WFNS) or Hunt and Hess I–III) present with adequate levels of alertness and often they have no major early cardiopulmonary complications, with the exception of acute hypertension. However, these patients can deteriorate rapidly because of development of hydrocephalus, seizures, or the occurrence of rebleeding. Thus, they demand close neurological monitoring. Patients with poor clinical grade aSAH (WFNS or Hunt and Hess IV–V) present with stupor or coma and their prevalence of neurogenic cardiopulmonary injury is high. They generally require mechanical ventilation and may need acute treatment because of global brain edema with or without hydrocephalus.

The first step of management is to ensure that they have a secure airway, adequate ventilation and oxygenation, and an effective circulation. Isotonic fluids, analgesia, and antiemesis should be provided. Acute hypertension is very prevalent and it is recommended to reduce the systolic blood pressure below 160 mmHg based on observational data indicating that patients with higher systolic pressures have higher rates of rebleeding. However, blood pressure should be lowered gradually because sudden reduction can compromise the cerebral perfusion pressure, especially if the intracranial pressure is high.

Pulmonary edema is a common early complication and, consequently, patients with aSAH should have a chest X-ray and be monitored with pulse oximetry. When present, pulmonary edema may be neurogenic, cardiogenic, or share both mechanisms. Ventilation with positive end-expiratory pressure can lead to resolution of pure neurogenic pulmonary edema, but diuretics are necessary when a cardiogenic component is at play. Electrocardiographic changes (especially affecting repolarization, such as prolongation of the QTc interval or diffuse changes in the T waves) and small elevations in serum troponin concentrations are quite prevalent and often inconsequential. However, patients with poor-grade aSAH – particularly postmenopausal women – can develop stress-induced cardiomyopathy with depressed ventricular ejection function and manifestations of acute heart failure. Although the most common echocardiographic expression of stress-induced cardiomyopathy affects predominantly the apex and spares the base (thus known as apical ballooning syndrome or takotsubo cardiomyopathy), other forms of regional wall motion disturbances can occur. Coronary angiography is generally not necessary when the diagnosis of stress-induced cardiomyopathy is suspected in patients with severe aSAH and no antecedent coronary artery disease.

Hydrocephalus (communicating or obstructive) can be present upon presentation, but often develops during the first few hours. As it develops, the patient becomes less responsive, but the change is not sudden. Hypertension and bradycardia are common. Downward gaze can be seen as an expression of tectal compression from the dilated third ventricle. Although communicating hydrocephalus can be treated with lumbar drainage if preferred, obstructive cases demand ventriculostomy. Unlike the relatively silent and gradual manifestations of hydrocephalus, rebleeding presents much more dramatically. Posturing is common and often confused with seizures. Marked hypertension is associated first with tachycardia because of the massive sympathetic discharge, and then with bradycardia secondary to the intracranial hypertension.

True seizures can also occur in this acute phase, either upon aneurysm rupture or within the following hours. Estimates of seizure frequency vary across studies, but they are unquestionably much more common among patients with poor-grade aSAH. Prophylactic anticonvulsants are generally not recommended. If they are used, it is better to avoid phenytoin because of its association with poorer cognitive outcomes and its interaction with nimodipine.

Pharmacological treatment during this initial phase should include nimodipine for prevention of delayed ischemic damage [9]. Administration of an antifibrinolytic agent (tranexamic acid or aminocaproic acid) can reduce the risk of rebleeding if started promptly after aneurysm rupture and it is a safe therapy if only used for up to 72 h [10].

Following aneurysm treatment, patients often experience a short “honeymoon period” of relative stability after which secondary insults can occur. During this period, careful monitoring of neurological and hemodynamic functions is essential. Unfortunately, there are no ideal methods to achieve these goals.

We remain convinced that the neurological examination (when performed by an experience and attentive examiner) is the most reliable method to diagnose secondary brain insults in patients with aSAH. Consequently, we always try to maintain our ability to perform a complete neurological examination if at all feasible. That means we try to extubate patients early whenever the pulmonary condition allows weaning and we avoid sedation and minimize the use of opiates as much as possible. Multimodality monitoring is an appealing and pathophysiologically sound alternative in comatose patients. Multiple parameters can be monitored, as shown on Table 2. However, it is important to bear in mind that there is no evidence that treatment guided by the monitoring of any of these parameters (or any combination of them) improves outcomes in aSAH.