Despite the progress made in the diagnosis and management of aneurysmal subarachnoid hemorrhage (aSAH), it has remained a potentially life-threatening disease, with loss of productivity leading to social and financial losses. The recent development in diagnosis and intensive care therapy has decreased the fatality from aSAH. The Ottawa subarachnoid hemorrhage (SAH) criteria are extremely beneficial in detecting and distinguishing SAH from other causes of headaches. Furthermore, a computerized cerebral angiogram (CTA) diagnoses aSAH with high sensitivity and specificity. The Digital Subtraction Angiography (DSA) gives more accuracy about the morphology and orientation of the cerebral aneurysms. The severity of aSAH is assessed with various scores and the most frequently used one is the World Federation of Neurosurgeons Score (WFNS). The Early Brain Injury (EBI) from a ruptured cerebral aneurysm leads to raised Intracranial Pressure (ICP), hydrocephalus and/or seizures. The systemic complications of aSAH include cardiorespiratory and hormonal dysfunctions. The recent development in the management of aSAH patients begins with controlling the headache using multimodal analgesia. Following an aSAH, there will be severe hypertension, which should be treated with short-acting antihypertensives to avoid rebleeding. The ruptured aneurysm should be repaired within 24 to 72 hours. The hydrocephalus should be managed by cerebrospinal fluid (CSF) diversion via an Extra-ventricular Drain (EVD). Witnessed seizures in aSAH patients should be treated with a short course of anticonvulsants. Delayed Cerebral Ischemia (DCI) should be prevented and minimized. More recently, the cerebral vasospasm can be detected by daily Transcranial Doppler (TCD), continuous electroencephalography (cEEG), CTA, and DSA. Prompt management of cerebral vasospasm by inducing hypertension, euvolemia, and keeping serum sodium at the high-normal range is essential for minimizing the occurrence of DCI. The cerebral vasospasm resistance to this therapy is increasingly treated with chemical or balloon-assisted cerebral angioplasty. Cardiac complications in aSAH patients range from arrhythmias to acute myocardial infarction, are diagnosed early by continuous monitoring, a series of ECGs, and cardiac biomarkers, and are treated immediately. The respiratory complications in aSAH include neurogenic pulmonary edema, aspiration, ventilator-associated pneumonia (VAP), and acute respiratory distress syndrome (ARDS). These should be treated with diuretics, inotropes, early intubation, a VAP prevention bundle, and lung protective ventilation. The electrolyte disturbance and metabolic complications of aSAH such as fever, hyperglycemia, and hyponatremia are detected early with intensive care therapy and managed accordingly. Early mechanical thromboprophylaxis with the addition of pharmacological prophylaxis as soon as the aneurysm is secured has led to a significant decrease in the incidence of deep vein thrombosis as well as pulmonary embolism.
