Intracranial hypertension management

Electrolyte balance In a retrospective review of 47 patients with refractory intracranial hypertension managed with thiopental coma, 42 patients had hypokalemia on induction and 16 had hyperkalemia on withdrawal of thiopental [46 ]. The median time to onset of hypokalemia was 11 hours, and the median time to the individual lowest value was 25 hours. The median time to peak hyperkalemia was 31 hours. All of those with hyperkalemia had previously had hypokalemia, and the degree of hyperkalemia correlated with the mean dose of potassium replacement. 

Management of Intracranial Hypertension (Intracranial Pressure >20 mmHg)... 

A 13-year-old boy underwent a 17-hour craniotomy in an attempt to resect an arteriovenous malformation with propofol-based anesthesia. He developed frank propofol infusion syndrome after 74 hours of postoperative propofol sedation in the neurosurgical ICU (used to manage intracranial hypertension). Echocardiography showed severe biventricular dysfunction despite extraordinary pharmacological support. Extracorporeal circulation with membrane oxygenation (ECMO) was instituted at the bedside via cannulation of the left femoral vessels. Hemofiltration... 

A 44-year-old woman was given ephedrine intravenously, to manage hypotension during spinal anesthesia. She developed intracranial hypertension and focal cerebral deficits related to multiple hemorrhagic cerebral infarcts. Angiography showed reversible beading, consistent with cerebral arteritis. 

Nonspecific pharmacologic treatment in the management of intracranial hypertension should include analgesics, sedatives, antipyretics, and paralytics under selected circumstances. 

Specific pharmacologic treatment in the management of intracranial hypertension includes mannitol, furosemide, and high-dose pentobarbital. Neither routine use of corticosteroids nor aggressive hyperventilation (i.e., Paco2 <25 mm Hg) should be used in the management of intracranial hypertension. 

The use of analgesics, sedatives, and paralytics has an important primary role in the management of intracranial hypertension (Fig. 56-3). This is related directly to the association of pain. 

Hypothermia extends the survival time and prevents the development of brain edema in rats with ALE, caused by hepatic devascularization and mild hypothermia (33—35°C), reduces ammonia-induced brain swelling and increased intracranial pressure in portacaval-shunted rats administered ammonium salts. These findings have led to the successful use of mild hypothennia for the treatment of uncontrolled intracranial hypertension in patients with ALF (Jalan et al., 1999). Mechanisms so far identified that underhe the beneficial effect of hypothermia in ALF include reduced blood-brain transfer of ammonia, improved cerebrovascular hemodynamics and normafization of extracellular brain amino acid patterns (for review of these mechanisms, see Vaquero et al., 2005). Mild hypothermia also improves hepatic function in experimental toxic fiver injury (Vaquero et al., 2(X)7) Mild-to-moderate hypothermia has the potential to serve as an important strategy in the management of patients with ALF awaiting liver transplantation. 

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