**5. Complications and current treatment approaches**

During aneurysmal SAH, extravasation of high-pressure arterial blood in the subarachnoid space is associated with a sudden ICP increase that, if severe and sustained, may compromise cerebral perfusion, causing global cerebral ischemia and early brain injury. Recently, the treatment of hypertension in intracranial hemorrhage patients has been discussed with INTERACT and ATACH training. The American Heart Association/American Stroke Association and Neurocritical Care guidelines include mean arterial blood pressure monitor, unsafe aneurysm types, and 110 or 160 mm Hg (or both) of the systolic blood bridge. Remember to keep it below 180 mm Hg. After aneurysm treatment, these parameters should not be made in such a way that spontaneous high blood pressure may be beneficial [29, 42–44].

Intracranial hypertension (ICP of at least 20 mm Hg) is a relatively common complication of SAH, especially in patients presenting with poor neurological condition. Multiple factors such as cerebral edema, intraparenchymal hematoma, acute communicating hydrocephalus, intraventricular hemorrhage, aneurysm rerupture, complications related to aneurysm treatment, early brain injury, and DCI may contribute to the development of intracranial hypertension. High ICP is associated with severe regulation of brain metabolism, increased risk of neurological deterioration,

#### *Intensive Care Management in Cerebral Aneurysm and Arteriovenous Malformations DOI: http://dx.doi.org/10.5772/intechopen.89714*

and poor outcome, particularly in the absence of medical treatment. An ICP greater than 20 mm Hg is considered as an independent predictor of severe disability and death in aneurysmal SAH. Critical cerebral perfusion pressure levels (less than 70 mm Hg) are significantly associated with cerebral infarction after SAH [45–51].

If the autoregulation mechanism is intact when intracranial pressure rises, the body tries to keep the cerebral blood flow (CBF) constant. As the ICP rises, the brain perfusion pressure drops. Systemic vascular resistance decreases, and vasodilatation occurs at the limits of autoregulation to keep CBF stable. Cerebral blood flow is mainly regulated by arterial carbon dioxide tension (PaCO2). Abnormal PaCO2 levels are considered to cause major changes in CBF through vasoconstriction and vasodilation, respectively, possibly contributing to further brain injury [52–56].

Main management principles of intracranial hypertension after SAH are traditionally guided by the literature on traumatic brain injury, due to high numbers. It should be noted that pathophysiology is completely different in our scenario. The role of therapies such as hyperosmolar agents, hypothermia, barbiturates and decompressive craniotomy is not clear in SAH patients with intracranial hypertension resistant to first-line therapies. The first approach to elevated ICP is cerebral venous drainage, normoventilation (PaCO2: 35–40 mm Hg), and positioning bed height from 30° to 45°. During sedation and aspiration of tracheal secretions and physiotherapy, neuromuscular blocking agents should be added if necessary. However, the role of these drugs for ICP management has not been fully established, and some authors report that they may be more harmful than useful [57].

The use of hyperosmolar agents, such as mannitol and hypertonic saline, are current popular options in the treatment of high ICP in SAH.

Studies have shown that hypertonic saline is effective in controlling ICP and improving cerebral blood flow. The last treatment steps at highly resistant ICP include barbiturate, induced hypothermia, and decompressive craniectomy. Therapeutic hypothermia has been shown to be effective in controlling ICP in SAH but has not been shown to be associated with improved functional outcome and low mortality rates.

There are studies showing that hypertonic saline is more effective than mannitol in lowering ICP in traumatic brain injury. But however, there is no specific recommendation to select hypertonic saline or mannitol as the first line for patients with high ICP caused by traumatic brain injury [58–66]. Recent literature reports effectivity of hypertonic saline like mannitol in reducing of ICP in SAH. However further studies are needed to evaluate safest and optimal dose concentration and impact on improvement of outcomes.

Decompressive craniectomy, an important approach in refractory ICP in SAH patients, is often discussed in patients with poor prognosis. Decompressive craniectomy has been associated with decreased mortality, significant decrease in ICP, increased cerebral oxygenation, and increased cerebral metabolism in many studies. However, severe disability or death was also observed in patients undergoing decompressive craniectomy for refractory ICP [67–72].

The hemodynamic approach, known as triple H therapy, has played a very important role in SAH treatment for many years. However, its safety and efficacy are discussed due to complications that may develop. In patients with SAH, a bolus normal saline fluid application is known to increase cerebral blood flow in areas of cerebral ischemia. The main purpose of fluid treatment in SAH is to maintain euvolemia and normal circulating blood volume. It should be noted that uncontrolled hypervolemia and hemodilution do not improve cerebral oxygen formation and may cause adverse events [73–77].

Noradrenaline perfusion may be added to the treatment to provide normotension in cases where appropriate blood pressure is not achieved despite fluid replacement

or in conditions limiting fluid therapy such as heart failure. If the pathology persists after blood pressure therapy in neurological examination, intravenous angioplasty or salvage therapy with intravenous infusion may be helpful. Prophylactic use of angioplasty is not recommended. Cardiac complications after SAH may vary from benign electrocardiogram changes to cardiogenic shock. Positive troponin value is common after SAH and is considered a good indicator of left ventricular dysfunction, which increases the risk of hypotension, pulmonary edema, and cerebral infarction. Treatment is symptomatic and most patients have spontaneous recovery within 2 weeks. However, aggressive ICU management may be necessary for severely impaired left ventricular functions. Dobutamine, levosimendan, milrinone, and even an intra-aortic balloon pump may be added to the treatment to maintain cerebral blood flow. It is known that the risk of heart failure and pulmonary complications is much higher in patients with low-grade SAH. Hypovolemia and pulmonary edema are known to increase the risk of delayed cerebral ischemia in this patient group. Long-term intensive care hospitalization may be required in SAH patients. This may result in pulmonary complications such as hospital-acquired pneumonia, cardiogenic or neurogenic pulmonary edema, aspiration pneumonia, and pulmonary embolism, which occurs in approximately 30% of patients.

Acute respiratory distress syndrome occurs in 27% of SAH patients and is an independent predictor of outcome. However, diuretics can be dangerous because of the risk of brain ischemia caused by hypovolemia. Early pulmonary edema and late pulmonary edema after SAH are caused by heart failure and inflammatory (i.e., non-cardiogenic) conditions, respectively.

Measurement of extravascular lung water index, cardiac index, and pulmonary vascular permeability index with Pulse Contour Cardiac Output (PiCCO) is considered to be useful in the identification of pulmonary edema in SAH patients [78–95]. Neither statin therapy nor magnesium infusions should be initiated for delayed cerebral ischemia. Cerebral vasospasm is just one component of delayed cerebral edema.

Hyponatremia is common in subarachnoid hemorrhage and is associated with longer hospitalization time, but not increased mortality. Sodium abnormalities are common and carry a risk of poor prognosis in acute SAH patients. We performed a 10-year observational sodium study. Hyponatremia was defined as serum sodium (sNa) concentration below 135 mmol/L, whereas hypernatremia as sNa above 150 mmol/L. Our 10-year targeted sodium management regimen in acute SAH patients showed that dysnatremias were frequent, predominantly hyponatremic state, due to cerebral salt wasting syndrome (CSW) and not syndrome of inappropriate antidiuretic hormone secretion (SIADH). Hypernatremia was shown to be an independent risk factor for inpatient mortality and poor outcome. The standard sodium protocol lowered the frequency of SIADH, which was encountered in only one patient over 5 years. However, it did not significantly reduce the incidence and outcome improvement of hyponatremia. Hypernatremia occurred more often and had a higher mortality and worse outcome than hyponatremia, but these patients were neurologically worse upon its onset. Hyponatremia is the most common electrolyte imbalance that occurs in 50% of patients after SAH. Two mechanisms are accepted for hyponatremia after SAH: CSW and SIADH. Cerebral salt wasting syndrome and SIADH have different pathogenesis. However, it is not always easy to distinguish in the clinic, and they can be observed in the same patient [96–100].

*Intensive Care Management in Cerebral Aneurysm and Arteriovenous Malformations DOI: http://dx.doi.org/10.5772/intechopen.89714*
