Observation in an ICU or a similar setting is strongly recommended for at least the first 24 hours, since the risk of neurologic deterioration is highest and because the majority of patients with brainstem or cerebellar hemorrhage have a depressed level of consciousness requiring ventilatory support. 57, 58 Invasive arterial blood pressure, central venous pressure, and pulmonary artery catheter monitoring are invasive modalities that may be indicated in these patients. An external ventricular drain should be placed in patients with a depressed level of consciousness (GCS of 8 or less), signs of acute hydrocephalus or intracranial mass effect on CT, and a prognosis that warrants aggressive ICU care. 59 Additional acute physiologic derangements that require aggressive interventions include elevated ICP, hyperglycemia, hyperthermia, electrolyte imbalances, and seizure activity among others.
Large-volume ICH carries the risk of developing cerebral edema and high ICP, and the presence of IVH further increases the risk of mortality 60, 61 (see Figure 2-1). This effect is primarily related to the development of obstructive hydrocephalus and alterations of normal cerebrospinal fluid flow dynamics. Patients with large-volume ICH, intracranial mass effect, and coma may benefit from ICP monitoring, although this intervention has not been proved to benefit outcomes after ICH, 62, 63 initial cerebrospinal fluid (CSF) drainage may be a lifesaving procedure, particularly in the setting of hydrocephalus and IVH. 64 This technique allows for rapid clearance of CSF, improvement of ICP, and ICP/CPP monitoring. As a general rule, an ICP monitor or external ventricular drain (EVD) should be placed in all comatose ICH patients (GCS of 8 or less) with the goal of maintaining ICP less than 20 mm Hg and CPP greater than 70 mm Hg, unless their condition is so dismal that aggressive ICU care is not warranted. Compared to parenchymal monitors, EVDs carry the therapeutic advantage of allowing CSF drainage and have the disadvantage of a substantial risk of infection (approximately 10% during the first 10 days). 65
Sedation should be used to minimize pain, agitation, and decrease surges in ICP, and in general, many practitioners prefer sedative agents and nondepolarizing neuromuscular paralytic agents for RSI that do not have effects on ICP such as propofol, etomidate, cis-atracurium, and vecuronium. 37, 41, 66 Additionally, this patient's head should be positioned at 30-degree angle to minimize ICP and reduce the risk of aspiration or ventilator-associated pneumonia. In mechanically ventilated patients, the further need for head elevation should be guided by changing pulmonary and volume needs.
Additional advanced techniques for the management of elevated ICP have evolved from the experience in traumatic brain injury. Two different concepts for the management of ICP currently exist. The Lund concept assumes a disruption of the blood-brain barrier (BBB) and recommends manipulations to decrease the hydrostatic blood pressure and to increase osmotic pressures to favor the maintenance of the vascular compartment at the expense of a higher risk of ischemia. 67 The other concept, cerebral perfusion pressure (CPP) optimization (CPP = MAP – ICP) favors a maintenance of the CPP of 70 mm Hg or more to minimize reflex vasodilation or ischemia 68, 69 at the expense of potentially aggravating ICP. There is no prospective control trial addressing the superiority of either of these two different methods for ICP management after ICH.
Hyperosmolar therapy and hyperventilation should be used after sedation and CPP optimization fail to normalize ICP. 70 The initial dose of mannitol is 1.0 to 1.5 g/kg of a 20% solution, followed by bolus doses of 0.25 to 1.0 g/kg as needed to a target osmolarity of 300 to 320 mOsm/kg. Additional doses can be given as frequently as once an hour based on the initial response to therapy with the anticipation of a transient drop in blood pressure (BP). Hypertonic saline (HS), such as 0.5 to 2.0 mL/kg of 23.4% saline solution, can be used as an alternative to mannitol, particularly in the setting of shock and when CPP augmentation is desirable through a central venous line. 71 Hyperventilation is generally used sparingly in the ICU and for brief periods in monitored patients because its effect on ICP tends to last for only a few hours. Good long-term outcomes can occur when the combination of osmotherapy and hyperventilation is successfully used to reverse transtentorial herniation. 72
For cases of severe or intractable elevated ICP, barbiturates and induced therapeutic hypothermia are also effective tools to control refractory elevated ICP by decreasing cerebral metabolic activity, which translates into a reduction of the CBF, and fall of the ICP. These two techniques require expertise, advanced tools, and continuous monitoring of cerebral electrical activity, and it may be associated with significant complications. 73-75
Admission hyperglycemia is a potent predictor of 30-day mortality in both diabetic and nondiabetic patients with ICH. 76 In ischemic stroke, hyperglycemia occurs in 20% to 40% of patients and is associated with infarct expansion, worse functional outcome, longer hospital stays, higher medical costs, and an increased risk of death, and it is felt to be secondary to a catecholamine surge and generalized stress response. 77-79 In the critically ill population, hyperglycemia seems much more acutely toxic than in healthy individuals, for whom cells can protect themselves by downregulation of glucose transporters. 80 In a recent study, high serum glucose concentrations were related to lower scores on the admission GCS and to unfavorable clinical outcomes, 81 but episodes of hypoglycemia have also been associated with increased mortality 82 and worst outcomes in neurologic patients, 83 even though in strict clinical environments tight glucose control has been linked to reductions in intracranial pressure, duration of mechanical ventilation, and seizure activity in critically ill neurologic patients. 84 Thus, to minimize the risk of severe hypoglycemia and to avoid worsening possible neuronal damage related to hyperglycemia, it may be reasonable to have tight sugar control with targets between 100 and 150 mg/dL.
Fever after ICH is common, particularly with IVH, 85 and should be treated aggressively. Sustained fever after ICH has been shown to be independently associated with poor outcomes. 86 A large body of experimental evidence indicates that even small degrees of hyperthermia can exacerbate ischemic brain injury 87, 88 as brain temperature elevation has been associated with hyperemia, exacerbation of cerebral edema, and elevated ICP. 89, 90 As a general standard, acetaminophen and cooling blankets are recommended for all patients with sustained fever in excess of 38.3°C (101oF) 73, 91 despite the lack of prospective randomized controlled trials supporting this approach. Newer adhesive surface-cooling systems (Arctic Sun, Medivance Inc, Lousville, CO, USA) and endovascular heat exchange catheters (Cool Line System, Alsius, Inc, Chelmsford, MA, USA) have been shown to be much more effective for maintaining normothermia 92 ; however, it remains to be seen if these measures can improve clinical outcome.
Isotonic fluids such as 0.9% saline at a rate of approximately 1 mL/kg per hour should be given as the standard intravenous replacement fluid for patients with ICH and optimized to achieve euvolemic balance and an hourly diuresis of > 0.5 mL/kg. Free water given in the form of 0.45% saline or 5% dextrose in water can exacerbate cerebral edema and increase ICP because it flows down its osmotic gradient into injured brain tissue. 44 Systemic hyposmolality (> 280 mOsm/L) should be aggressively treated with mannitol or 3% hypertonic saline. A state of euvolemia should be maintained by monitoring fluid balance and body weight, and by maintaining a normal central venous pressure (range 5 to 8 mm Hg). Careful interpretation of the CVP should be done when analyzing its value in the setting of positive end-expiratory pressure (PEEP). The use of hypertonic saline in the form of a 2% to 3% sodium (50:50 chloride-acetate) solution (1 mL/kg per hour) has become an increasingly popular alternative to normal saline as a resuscitation fluid for patients with significant perihematomal edema and mass effect after ICH. The goal is to establish and maintain a baseline state of hyperosmolality (300 to 320 mOsms/L) and hypernatremia (150 to 155 mEq/L), which may reduce cellular swelling and the number of ICP crises. Potential complications of hypertonic saline use are encephalopathy, subdural hematomas, coagulopathy, fluid overload, hypokalemia, cardiac arrhythmias, and hyperchloremic metabolic acidosis. 93 The serum sodium level should never be allowed to drop more than 12 mEq/L over 24 hours, as rapid withdrawal of hypertonic therapy may result in rebound cerebral edema, leading to elevated ICP and/or herniation syndromes. 93, 94
Seizures should be treated with intravenous lorazepam (0.05 to 0.1 mg/kg) followed by a loading dose of phenytoin or fosphenytoin (20 mg/kg). Patients with ICH may benefit from prophylactic antiepileptic therapy (AED), but no randomized trial has addressed the efficacy of this approach. The American Heart Association guidelines have recommended antiepileptic medication for up to 1 month, after which therapy should be discontinued in the absence of seizures. 43 This recommendation may be supported by the results of a recent study that showed that the risk of early seizures was reduced by prophylactic AED therapy. 95 The 30-day risk for convulsive seizures after ICH is approximately 8%, and the risk of overt status epilepticus is 1% to 2%. 95 Lobar location and small hematomas are independent predictors of early seizures. 95 The argument for prophylactic anticonvulsant therapy in stuporous or comatose ICH patients is bolstered by the fact that continuous EEG monitoring demonstrates electrographic seizure activity in approximately 25% of these patients despite treatment. 96, 97 The risk of late seizures or epilepsy among survivors of ICH is 5% to 27%. 95
Deep Venous Thrombosis Prophylaxis
Patients with ICH are at high risk for deep vein thrombosis (DVT) and pulmonary embolism, a potentially fatal complication, due to limb paresis and prolonged immobilization. Dynamic compression stockings should be placed on admission. 98 A small prospective trial has shown that low-dose subcutaneous heparin (5000 U bid) starting after the second day significantly reduced the frequency of venous thromboembolism with no increase in intracranial bleeding. 99 Treatment with low-molecular-weight heparin (ie, enoxaparin 40 mg daily) is a reasonable alternative if renal function is normal. It is generally safe to initiate the DVT prophylaxis after ICH after the first 24 to 48 hours provided that there is no active bleeding or hematoma expansion in progress nor any underlying coagulopathy.
As is the case with all critically ill neurologic patients, enteral feeding should be started within 48 hours to avoid protein catabolism and malnutrition. A small-bore nasoduodenal feeding tube may reduce the risk of aspiration events.