FACTORS CAUSING FLUID AND ELECTROLYTE DISTURBANCES IN THE NEUROSURGICAL PATIENT

✅POOR ORAL INTAKE LEADING TO DEHYDRATION DUE TO

🔖 Decreased conscious level

🔖 Vomiting

🔖 Bulbar dysfunction 

🔖 Pending surgery 

✅FLUID OVERLOAD DUE TO

🔖overzealous intravenous rehydration 

✅DRUGS

🔖osmotic or loop diuretic therapy as part of the management of raised ICP

✅DISORDERS OF SODIUM-WATER BALANCE ASSOCIATED WITH THE NEUROLOGICAL PATHOLOGY/ SURGERY

🔖Syndrome of inappropriate antidiuretic hormone secretion (SIADH)

🔖Cerebral salt wasting (CSWS) 

🔖Diabetes insipidus

PAIN IN GUILLAIN BARRE SYNDROME

✔️GBS a number of different subtypes

✔️The most common is an acute inflammatory demyelinating polyradiculoneuropathy 

✔️More than half of patients report severe pain. 

✔️Severe widespread neuropathic pain may be described, often without the features of a peripheral neuropathy, as well as musculoskeletal pain. 

✔️May sometimes have severe acute pain, 

✔️Treatment with systemic ketamine and/or lidocaine as well as gabapentin/pregabalin and carbamazepine may be of benefit in the acute phase (ANZCA and FPM, 2010).

Ref: Acute Pain Management: A practical guide,4/e, Pamela E. Macintyre , Stephan A. Schug

💹EEG IN ACUTE INTOXICATIONS

💠Barbiturates 

Usually they produce fast activity (15-35/sec ) In the acute overdose, these type of fast activity may still be present, with some deceleration (10-16/sec). The inability of the cortex to produce, barbiturate induced fast activity has been described as a sign of cerebral impairment 

💠Benzodiazepines 

〰Fast activity (15-25/sec) range

💠Tricyclic Antidepressants

〰Widespread and poorly reactive 8-10/sec activity with paroxysmal discharges

💠Lithium Carbonate

〰Marked slowing, paroxysmal bursts, and triphasic waves

💠Neuroleptic drugs ( phenothiazines, butyrophenones)

〰Diffuse slow activity; often with burst like appearance or intermingled with paroxysmal discharges. Fast frequencies are absent

💠Opioids:

〰Relatively little repercussion in EEG; if produces profound coma → diffuse slowing

💠Carbon monoxide

〰Massive slowing (1-4/sec)

💠Ethyl alcohol

〰Effect on EEG is mild

💠Methyl alcohol

〰EEG slowing is correlated with acidosis rather than blood and CSF methanol levels

💠Organophosphorous compounds

〰Initially, fast EEG activity may be supplanted by slow activity 

Ref: EEG and intensive care medicine : RB Hansen, E Niedermeyer; Prog neurol Surg, vol 12, pp 105-145 ( Karger, Basel 1987)