Oedema cerebral

A series of 4-arylpyrimidines that arc amine substituted at pyrimidine C-2 was prepared. FK360 was most effective from this group on both arachidonate-induced cerebral oedema in rats and as an in vitro inhibitor of lipid peroxidation. The authors link effects of FK360 to the arachidonic acid cascade (Kuno et al., 1992). This is an unusual structure. 

Paracetamol overdose is most likely to cause hepatic necrosis and to a lesser extent renal necrosis. Hepatic necrosis is maximal within 3-4 hours of ingestion and may lead to encephalopathy, haemorrhage, hypoglycaemia, cerebral oedema and death. Acetylcysteine tends to protect the liver if given within 10-12 hours of paracetamol poisoning. The maximum adult dose of paracetamol is 4 g in 24 hours. 

Dexamethasone Synthetic glucocorticoid, lacks mineralocorticoid activity Used to treat range of inflammatory diseases. Used to treat some forms of asthma, also cerebral oedema and congenital adrenal hyperplasia... 

The three main types of altitude illness, characterised initially by nausea, headache, sleep disturbance and stomach upset, are acute mountain sickness (AMS) high altitude pulmonary oedema (HAPE) and high altitude cerebral oedema (HACK). They occur after rapid ascent to altitudes greater than 2,500 m (about 8,000 feet) in unacclimatised people. In unacclimatised mountaineers, the prevalence of AMS at 4,559 metres (15,000 feet) is approximately 50% and HAPE 4%. Risk depends on individual susceptibility, rate of ascent and pre-exposure to high altitude. AMS is not a pre-requisite for HAPE. 

A. Disturbed consciousness may be due to cerebral oedema, if suspected give intravenous mannitol. Otherwise lactuiose or neomycin by mouth can help by reducing gutammonia loading. 

Fatty infiltration with cerebral oedema (Reye s syndrome) Aspirin... 

The mainstay of medical treatment is fluid restriction, but this may not be appropriate in the surgical and critical care patient population. Severe (<120 mmol-L-l) or symptomatic hyponatraemia (mental status changes, seizure) requires more aggressive therapy to reduce cerebral oedema. Infusion of hypertonic saline to increase plasma sodium concentrations to 120-125 mmol L-1 alleviates symptoms. Adjunct therapy with demeclocycline (600 mg-day-1) may assist management in resistant SIADH. Demeclocycline is a tetracycline antibiotic which inhibits the actions of ADH at the renal tubules. 

Azzopardi J, Gatt A, Zammit A, Alberti G. Lack of evidence of cerebral oedema in adults treated for diabetic ketoacidosis with fluids of different tonicity. Diabetes Res Clin Pract 2002 57(2) 87-92. 

Lebl J, Kolska M, Zavacka A, Eliasek J, Gut J, Biolek J. Cerebral oedema in enuretic children during low-dose desmopressin treatment a preventable complication. Eur J Pediatr 2001 160(3) 159-62. 

McIntosh, T., Banbury, M. and Smith, D. (1992) The novel 21-aminosteroid U74006F attenuates cerebral oedema and improves survival after brain injury in the rat, Acta Neurochir. 51(Suppl), 329-330. 

Tumour necrosis factor-a (TNFa) accumulates in the brain after trauma. This cytokine is known to be an important factor in delayed CNS damage. It was found that, in addition to its anti-NMDA effect, HU-211 causes up to 90% inhibition of the TNFa surge after closed head injury in rats [195], Bacterial and viral infections of the CNS are known to cause secretion of the TNFa as well as interleukin-1 and other cytokines which are involved in the inflammatory process and may cause secondary damage. Such infections may result in high mortality. It was found that rats infected with Streptococcus pneumoniae suffered less cerebral oedema on treatment with a combination of a suitable antibiotic with HU-211 than the antibiotic alone [196],... 

O Connor A, Cluroe A, Couch R, Galler L, Lawrence J, Synek B. Death from hyponatraemia-induced cerebral oedema associated with MDMA ( ecstasy ) use. NZ Med J 1999 112(1091) 255-6. 

ST JOHN S WORT CORTICOSTEROIDS 1 plasma concentrations of corticosteroids and risk of poor or inadequate therapeutic response, which would be undesirable if used for e.g. cerebral oedema Due to induction of the hepatic metabolism by the CYP3A4 isoenzymes Monitor therapeutic response closely -clinically, with ophthalmoscopy and radiologically - and t dose of corticosteroids for desired therapeutic effect... 

Adverse reactions include gastrointestinal symptoms, conjunctivitis and vertigo. More serious effects are erythema multiforme, haemolytic anaemia, agranulocytosis, cerebral oedema and hepatitis. 

Cj sctcerccsis Taenia. llbcildaiole or praiiquniitol Treat in hospital as dying and disintegrating cysts may cause cerebral oedema... 

Acetic acids. Indomethacin may cause prominent salt and fluid retention. Headache is coiiunon, often similar to migraine, and is attributed to cerebral oedema it can be limited by starting at a low dose... 

Headache of raised intracranial pressure (cerebral oedema) responds to dexamethasone (10 mg i.v. 4 mg 6-hourly, 2-10 d) which reduces the pressure and to nonopioid anedgesics (see also Palliative care). 

Acute mountain/altitude sickness, to reduce cerebral oedema. 

Raised intracranial pressure due to cerebral oedema, e.g. in cerebral tumour or encephalitis (probably an anti-inflammatory effect which reduces vascular permeability and acts in 12-24 h) give dexamethasone 10 mg i.m. or i.v. (or equivalent) initially and then 4 mg 6-hourly by the appropriate route, reducing dose after 2-4 days and withdrawing over 5-7 days but much higher doses may be used in palliation of inoperable cerebral tumour. 

Success in treatment of diabetic ketoacidosis and its complications (hypokalaemia, aspiration of stomach contents, infection, shock, thromboembolism, cerebral oedema) depends on close, constant, informed supervision. 

Buiiimore, D. The role of polyamines in hepatic encephalopathy and cerebral oedema. Europ. X. Gastroenterol. Hepatol. 1993 5 63-67... 

Clinically, there are three different courses of disease following the onset of jaundice .) fulminant or hyperacute liver failure (= occurrence of hepatic encephalopathy in the 1 week), (2.) acute liver failure (= occurrence of hepatic encephalopathy between the and 4 week), and (5.) subacute liver failure (= occurrence of hepatic encephalopathy between the 5 and 8 week). Surprisingly, however, it could be shown that 30-40% of the hyperacute forms survived in spite of the development of hepatic coma and cerebral oedema. As opposed to this, the subacute forms displayed a survival rate of only 10-20%, despite a lower frequency of cerebral oedema and better liver function, (s. tab. 20.1)... 

Circulatory disorders In general, acute liver failure is initially accompanied by hyperdynamic circulation. During the further course, approx. 80% of patients develop hypotension, which above all results in a considerable reduction in hepatic, cerebral and renal perfusion. At the same time, peripheral vasodilation is usually witnessed. Bradycardia, generally resulting from cerebral oedema, worsens the cardiovascular conditions and is considered to be a poor prognostic sign. Ultimately, the patient does not respond to volume expansion and catecholamines. 

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