Brain edema treatment

Modern diuretics (natriuretics, saluretics), as used in the treatment of hypertension and heart failure, are administered with the aim to enhance the renal excretion of sodium ions and water. Older diuretics, such as the osmotic diuretic agents, are of little interest in the treatment of the aforementioned cardiovascular disorders, but may be used to lower intracranial pressure associated with brain edema. 

Conventional treatment of raised ICP in this condition consists of artificial ventilation, osmotherapy, and barbiturate administration. The value and duration of these measures has come under scrutiny. Prolonged hyperventilation has been discouraged, as the potential decrease in cerebral arterial blood flow resulting from additional hypocarbia might exacerbate tissue ischemia (34). Early use of agents such as glycerol or mannitol, at least in theory, may actually hasten tissue shifts and therefore lead to an aggravation of brain edema (35). Barbiturate therapy has to date failed to prove to be of therapeutic benefit in the treatment of postischemic brain edema (36). 

In conclusion, induced, moderate hypothermia can decrease ICP, reduce mortality, and may improve outcome in patients with severe MCA infarction with malignant postischemic brain edema. Important side effects are reduction of platelet count, increased rate of pneumonia, and elevation of serum amylase and lipase levels. The results of our own pilot trial suggest a beneficial effect of moderate hypothermia in the treatment of severe space-occupying MCA infarction. However, our data call for a randomized trial of hypothermia in the therapy of malignant MCA infarction. Whether early hypothermic therapy within the first 6 h after onset of symptoms can reduce infarct size has to be clarified in further clinical trials. 

These include mannitol and sorbitol which act mainly in the proximal tubules to prevent reabsorption of water. These polyhydric alcohols cannot be absorbed and therefore bind a corresponding volume of water. Since body cells lack transport mechanisms for these substances (structure on p.175), they also cannot be absorbed through the intestinal epithelium and thus need to be given by intravenous infusion. The result of osmotic diuresis is a large volume of dilute urine, as in decompensated diabetes melli-tus. Osmotic diuretics are indicated in the prophylaxis of renal hypovolemic failure, the mobilization of brain edema, and the treatment of acute glaucoma attacks (p. 346). 

Synthesis of(RVfluorenylo acetic acid, useful in the treatment of brain edema... 

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. 

A transient encephalopathy has been reported after the use of an iodinated contrast medium in a neurointerventional procedure with development of psychomotor agitation, disorientation, and progressive left faciobrachial hemiparesis 30 minutes after successful treatment of a right carotid-ophthalmic fusiform aneurysm [6 ]. A CT scan showed marked cortical enhancement and edema in the right cerebral hemisphere, thought to be due to contrast extravasation after disruption of the blood-brain barrier. Treatment with dexa-methasone and maimitol produced complete recovery. 

The goals of treatment of brain metastases are to manage symptoms by reducing cerebral edema, treat the underlying malignancy both locally and systemically, and improve survival. 

Patients with acute stroke should be monitored intensely for the development of neurologic worsening, complications, and adverse effects from treatments. The most common reasons for clinical deterioration in stroke patients are (1) extension of the original lesion in the brain (2) development of cerebral edema and raised intracranial pressure (3) hypertensive emergency (4) infection (e.g., urinary and respiratory tract) (5) venous thromboembolism (6) electrolyte abnormalities and rhythm disturbances and (7) recurrent stroke. The approach to monitoring stroke patients is summarized in Table 13-3. 

Dexamethasone Testing of adrenal cortical hyperfunction cerebral edema associated with primary or metastatic brain tumor, craniotomy, or head injury. Tnamc/no/one Treatment of pulmonary emphysema where bronchospasm or bronchial edema plays a significant role, and diffuse interstitial pulmonary fibrosis (Hamman-Rich syndrome) in conjunction with diuretic agents to induce a diuresis in refractory CHF and in cirrhosis of the liver with refractory ascites and for postoperative dental inflammatory reactions. 

The TET-induced inhibitory influence on cyclic 3 ,5 -AMP phosphodiesterase (PDE) activities precedes edema formation in the rat brain [74]. lb clarify the mechanism of the protective action of EGb against TET-toxidty in rats, in vitro and ex vivo effects of EGb on PDE activities of cerebral tissue were investigated [75]. Higher concentrations of EGb (5-250 mg/L) inhibited the PDE activity in the brain in normal rats, whereas lower concentrations (0.25-4.0 mg/L) of EGb enhanced the activity of the enzyme. The inhbitory effect of TET on the high affinity PDE activity (measured with 0.25 ftM cyclic AMP) of the brain was diminished in the presence of low EGb concentrations. Furthermore, preventive and curative treatment of 1 El-poisoned rats with EGb (100 mg/kg, p.o., for 7 days) prevented both the formation of edema and the fall of PDE activity induced by TET alone. These results suggested the antiedema action of EGb might be partly associated with its modulating influences on cellular cyclic AMP levels via activation of membrane-bound PDE. 

Of 143 patients (62) studied retrospectively, eight stopped taking treatment because of significant peripheral edema, one had an exacerbation of cardiac failure, and one reported myalgia. HbAlc, lipid profiles, and blood pressure improved. In 38 patients taking pioglitazone brain natriuretic peptide, which may play a role in fluid retention, did not rise (63). 

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