Cerebral edema treatment

It has been shown that arachidonic acid metabolism could contribute to the pathogenesis of cerebral edema. Treatment with indomethacin, a COX inhibitor, nordihydroguaiaretic acid, a LOX inhibitor, or their combination significantly reduced vasogenic edema induced by freezing lesions (Yen and Lee, 1987). 

Mannitol (Osmitrol) is used for the promotion of diuresis in the prevention and treatment of the oliguric phase of acute renal failure as well as for the reduction of IOP and the treatment of cerebral edema Urea (Ureaphil) is useful in reducing cerebral edema and in die reduction of IOE Glycerin (Osmoglyn) and isosorbide (Ismotic) are used in the treatment of acute glaucoma and to reduce IOP before and after eye surgery. 

Qureshi A, Suarez JI. Use of hypertonic saline solutions in treatment of cerebral edema and intracranial hypertension. Crit Care Med 2000 28(9) 3301-3313. 

Acute complications of stroke include cerebral edema, increased intracranial pressure, seizures, and hemorrhagic conversion. In the acute setting, several supportive interventions and treatments to prevent acute complications should be initiated. 

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. 

The cerebral edema produced by sublethal doses of bromethalin can be ameliorated by treatment with an osmotic diuretic and corticosteroids. Pathology from sublethal doses, even without treatment have been shown to be reversible. 

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. 

Extravasation of polymorphonuclear leukocytes (PMNs) in the area of injury occurs very early after injury in several different models of experimental TBI, and has been shown to correlate with the development of cerebral edema (101,102). Early canine studies conducted by Rosomoff (16,57) demonstrated that treatment with hypothermia decreased the posttraumatic cellular inflammatory response incited by experimental head injury compared to normothermic controls. This effect of hypothermia is likely mediated by several mechanisms including preservation of the BBB, thereby limiting extravasation of inflammatory cells and mediators into the area of injury (103), suppressing release of cytokines (22), and reducing CBF. 

Hypothermia is known to cause cardiac dysfunction, particularly arrhythmias (36,37). Careful temperature control and optimal antiar-rhythmic therapy can minimize this problem. However, to avoid severe circulatory dysfunction, knowledge of arrhythmias is required. Hypothermia may be associated with a suppression of the immunological system, which exposes patients to the danger of severe infections. Schwab et al. reported that 7 of 25 stroke patients undergoing hypoth-ermiatherapy suffered a septic syndrome (17). In our hypothermic study, none of the 13 patients who underwent hypothermia therapy for 3-7 d developed severe infectious diseases. However, the remaining patient, who underwent 10 d of hypothermia because of massive cerebral edema, developed septic shock on the 10th day of hypothermia treatment. The immunosuppressive effect appears to be correlated with the depth and... 

For parenteral administration in intensive therapy or in emergendes, the sodium phosphate ester may be given intravenously by injection or infusion, or intramuscularly by injection. Dexamethasone sodium phosphate is also used in the treatment of cerebral edema caused by malignancy. The sodium phosphate ester is given by intra-articular, intra-lesional or soft tissue injection. Dexamethasone acetate may be given by intramuscular injection in conditions where corticosteroid treatment is indicated, but a prompt response of short duration is not required. 

A healthy 19-year-old woman complained of nausea and vomited 8 hours after taking unknown quantities of MDMA and beer 3 hours later, she suddenly clenched her jaw, had tonic contractions of all four limbs, and collapsed. She was obtunded, with occasional moaning and non-purposeful movements of the limbs. Head CT scan showed mild cerebral edema. Her serum electrolytes, including a sodium of 115 mmol/1 and a corresponding urine osmolality of 522 mosm/kg, suggested SIADH. Despite treatment, the serum sodium concentration 10 hours later was 116 mmol/1, but 18 hours after treatment, it rose to 125 mmol/1. She became progressively more responsive, with normalization of her sodium concentration, and after 48 hours was awake and alert, with a serum sodium concentration of 136 mmol/1. 

Current practice has dictated the treatment of cerebral edema in patients. The two treatments most commonly used are osmotic agents and steroids. The key to the treatment of cerebral edema, which is still empirical, is the accurate identification of... 

Very rarely, in cases of neurocysticercosis, the reaction of the nervous system to the death of the parasite is extremely violent. In one case cerebral edema resulted in permanent neurological damage (22), while other patients have suffered hydrocephalus or acute intracranial hypertension requiring treatment, for example with glucocorticoids or mannitol (23). 

Only six of 36 children who took overdoses of co-phenotrope had signs of atropine overdose (central nervous system excitement, hypertension, fever, flushed dry skin) (1). Opioid overdose (central nervous system and respiratory depression with miosis) predominated or occurred without any signs of atropine toxicity in 33 cases (92%). Diphenoxylate-induced hjrpoxia was the major problem and was associated with slow or fast respiration, hypotonia or rigidity, cardiac arrest, and in three cases cerebral edema and death. Respiratory depression recurred 13-24 hours after the ingestion in seven cases and was probably due to accumulation of difenoxine, an active metabolite of diphenoxylate. Recommended treatment is an intravenous bolus dose of naloxone, followed by a continuous intravenous infusion, prompt gastric lavage, repeated administration of activated charcoal, and close monitoring for 24 hours. 

Therapeutically, mannitol administered parenterally is used as an osmotic diuretic, as a diagnostic agent for kidney function, as an adjunct in the treatment of acute renal failure, and as an agent to reduce intracranial pressure, treat cerebral edema, and reduce intraocular pressure. Given orally, mannitol is not absorbed significantly from the GI tract, but in large doses it can cause osmotic diarrhea see Section 14. 

Glucocorticoids are recommended for the treatment of CNS disorders as they stabilize microvas-cular permeability, reduce edema formation, reduce intracranial pressure, decrease oxygen-derived free radicals and prevent post-traumatic autodestruction of nervous tissue. Their clinical use in equine medicine includes the treatment of brain and spinal cord trauma, cerebral edema associated with neonatal maladjustment syndrome (NMS), endotoxic shock and EPM. This is despite the fact that the safety and efficacy of glucocorticoids in the treatment of many types of nervous system inflammation has not been established and their use and dosing schedules continue to be debated. 

The organic solvent dimethyl sulfoxide (DMSO) has a wide range of pharmacological actions Qacob Herschler 1986). The intraarticular use of this agent is discussed in Chapter 7. A short discussion on DMSO including its use in the treatment of CNS trauma and cerebral edema in horses is included here. 

Mannitol, the most commonly employed osmotic diuretic, is a large polysaccharide molecule. It is often selected for use in the prophylaxis or treatment of oliguric ARF. It is not absorbed from the gastrointestinal tract and, therefore, is only administered i.v. with its elimination dependent on the GFR (within 30 to 60 min with normal renal function). Mannitol is distributed within the plasma and extracellular fluid spaces and produces an increase in the serum osmolality and expansion of the circulating volume. It is not generally used for the treatment of edema because any mannitol retained in the extracellular fluid can promote further edema formation. Furthermore, acute plasma volume expansion may challenge individuals with poor cardiac contractility and can precipitate pulmonary edema. Mannitol is commonly administered for the treatment of cerebral edema consequent to head trauma or to hypoxic-ischemic encephalopathy in neonatal foals. Because mannitol promotes water excretion, hypernatremia is a potential complication in patients that do not have free access to water (Martinez-Maldonado Cordova 1990, Wilcox 1991). 

An alternative is a solution of 2.5% dextrose and 0.45% sodium chloride (85Kcal/L), which, once the dextrose has been metabolized, has an effective osmolality one-half of that of plasma. It is retained better in e circulation (20% after 30 min compared with 10% for D5W) (Spalding Goodwin 1999) and can be used in the treatment of moderate plasma hypertonicity or when plasma glucose concentration is a concern. It should be noted that a rapid reduction in plasma tonicity has been associated with the development of cerebral edema, resulting in coma, seizures and death in other species (Adrogue Madias 2000a). This has not been documented in the horse. 

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