Stroke patients who require ICU admission most commonly do so because of concerns of cerebral edema and possible neurological deterioration, and several general measures may be undertaken to minimize the likelihood of developing these complications. Head of bed elevation to 30° helps to reduce ICP and allows for more unimpeded return of venous blood to the heart. Some of the earliest work on head of bed elevation in brain injured patients was by Rosner and Coley,10 who studied 18 patients with ICP elevations, and found that for every 10° of head elevation above the horizontal position the ICP decreased by an average of 1 mm Hg; however, the CPP also decreased by an average of 2-3 mm Hg. Adequate hydration and systemic blood pressure are essential to maintaining adequate CPP in this setting. Fan11 systematically reviewed studies of head of bed elevation with brain injuries, showing a consistent reduction in ICP across most studies. Meixensberger et al.12 evaluated the effect of head elevation on tissue perfusion, measuring local tissue po2 by a parenchymal microcatheter. They found that ICP could be significantly improved without compromising the regional cerebral oxygenation. The head should also be kept in the midline as much as possible, as significant head turning may cause venous compression in the neck, thereby increasing ICP. This was studied in neonates by Goldberg et al.,13 who found significant elevations in ICP when their heads were in the side position versus midline.
However, in patients with a flow-dependent state (e.g., basilar stenosis with a fluctuating exam), sometimes the head of bed should be kept flat, or even in the
Trendelenberg position, in order to help perfuse the ischemic brain regions. Wojner-Alexander et al.14 studied 20 stroke patients with transcranial Doppler (TCD) of the middle cerebral artery (MCA), measuring mean flow velocities (MFV) at 30°, 15°, and 0° head of bed elevation. The MFV improved in all patients by lowering the head of bed, and three patients demonstrated immediate neurological improvement when lowered to 0° .
The patient should be kept calm as much as possible, but this may be difficult if they are delirious, and sometimes the use of sedating medications is necessary. This carries with it the risk of confounding the neurological exam, which is vital to follow during this acute period when the patient is at risk for deterioration. Thus, short-acting medications in the lowest effective doses should be administered.
Fluid and electrolyte status requires special attention, and care should be given to avoid hypotonic fluids. In general, judicious fluid restriction should be used, as this will minimize cerebral edema. However, since stroke patients may present in a dehydrated state, which may predispose them to thrombosis, adequate isotonic fluids should be administered. Typical hydration orders include normal saline, with or without potassium supplementation, at a rate of 50-100 cm3/hour. The patient's serum sodium should optimally be kept in the 140-145 mmol/L range in the first few days following the stroke; the sodium may be manipulated to higher ranges later in the ICU course, should the patient require osmotic therapy. Glycemic control is of great importance, and fluids containing dextrose should generally be avoided. Continuous insulin infusions are more commonly being utilized in the Neurointensive Care Unit setting, often with a target serum glucose range of 80-120 mg/dL. Hyperglyce-mia has been associated with increased volumes of stroke (both in experimental animal models and in humans), increased cerebral edema, and worse neurological outcomes after stroke.15 An increased rate of hemorrhagic transformation following intravenous thrombolysis has also been found in association with hyperglycemia.16 Proposed mechanisms of injury include acidosis,17 increased excitotoxic amino acids,18 increased cerebral edema, and breakdown of the blood-brain barrier (BBB).19
Other electrolytes of importance include calcium (especially if the patient is receiving a calcium channel blocker, such as nicardipine) and magnesium, as hypo-magnesemia may predispose the patient to seizures, further complicating the ICP management. If the patient received intravenous iodinated contrast as part of their stroke evaluation, then careful monitoring of the blood urea nitrogen (BUN) and creatinine levels is necessary to detect contrast nephropathy.
Other general measures should be employed to prevent the development of common ICU complications. Stroke patients are at high risk for developing deep venous thrombosis (DVT), and prophylaxis should begin immediately upon admission to the ICU with compression stockings and pneumatic compression devices. Low-grade anticoagulation with subcutaneous heparin or low-molecular-weight heparin has also become a mainstay of treatment,20 but should be delayed for 24 hours after a patient has received intravenous recombinant tissue-plasminogen activator (rt-PA). In the setting of a rapid platelet drop, vigilant attention is needed to diagnose heparin-induced thrombocytopenia and thrombosis, and heparin-containing products may need to be avoided. H2-antagonists or proton pump inhibitors should be given to prevent gastritis/ulcer formation. Enteral feeding should begin as early as possible, either orally if the patient is able to swallow, or by the use of a nasogastric tube. However, if the patient is at high risk for possible respiratory decompensation with the need for intubation, or if invasive surgical procedures are planned, then feeding should be withheld. All stroke patients should have a formal swallowing evaluation to reduce the risk of aspiration pneumonia, the most common infectious complication in stroke patients. Frequent chest physical therapy and repositioning are also useful techniques. The second most common infectious complication is a urinary tract infection, and the use of indwelling catheters should be limited as much as possible in the individual patient. Finally, bed-bound stroke patients are at high risk for constipation and bowel obstruction, and stool softeners and bowel motility agents may be helpful in preventing these complications. Table 8.1 shows commonly used orders in the admission of stroke patients to the ICU.
Brain-injured patients commonly experience fever, and hyperthermia may correlate with poor outcome in these patients, although a direct causative link has yet to be established. The impact of fever on patients in a neurocritical care unit has been evaluated, and after controlling for severity of illness, diagnosis, age, and complications, increased body temperature was found to strongly associate with an increased length of ICU and hospital stay, as well as higher mortality and
TABLE 8.1 General Admission Orders for Stroke Patients to the ICU.
TABLE 8.1 General Admission Orders for Stroke Patients to the ICU.
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