💹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)

Nonthrombolytic therapy for patients who are not candidates for rTPA after ischemic stroke

TARGET: 

✔️optimization of CBF

✔️prevention of secondary brain injury, infarct extension & hemorrhagic conversion 

✔️avoid post-stroke complications (e.g., pulmonary embolus and aspiration pneumonia)

✔️ early mobilization and rehabilitation

✔️ attention to psychiatric ( e.g. Depression) and social consequences of stroke and assistance with daily activities.

(1) Airway management, hemodynamic monitoring, and treatment of increased ICP 

(2) aggressive antihypertensive therapy may exacerbate ischemia by decreasing CBF. A generally accepted cutoff for the administration of antihypertensive therapies is SBP >220 mm Hg, DBP >120 mm Hg, or MAP >130 mm Hg. 

(3) In the absence of hemorrhage on a CT scan, antiplatelet therapy is initiated in the form of aspirin starting with 325 mg by mouth followed by 81 to 160 mg daily.

(4) Multiple studies have failed to show a benefit to heparin administration ; but anticoagulation is usually initiated when atrial fibrillation is present.

(5) Hyperglycemia worsens neurologic outcome. So , euglycemia (80 to 110 mg/dL) is beneficial if it can be achieved without substantially increasing the risk of hypoglycemia.

(6) Seizures are treated with phenytoin, loading dose 15 mg/kg i.v. over 20 minutes followed by 5 to 7 mg/kg/day, or fosphenytoin, loading dose PE 15 to 20 mg/kg i.v., and then 4 to 6 PE mg/kg/day.

(7) DVT prophylaxis is provided using pneumatic compression or low-molecular-weight heparin e.g. enoxaparin, 0.5 mg/kg subcutaneously twice a day.

(8) After the evaluation of airway reflexes and adequacy of swallowing, nutrition is provided via a suitable route.

(9) A few studies suggest that positioning the head end of the bed at 15° for patients who have normal ICP improves CBF and neurologic function.

(10) Rehabilitation and psychiatric evaluation. e.g. Treatment of depression and other psychiatric comorbidities facilitates rehabilitation and improves functional status.

Ref: Seth Manoach, Jean G. Charchaflieh, Handbook of Neuroanesthesia, 4th Edition, Lippincott Williams & Wilkins

ANAESTHETIC IMPLICATIONS IN EPILEPSY SURGERIES

✔️If Awake Craniotomy/ wake up testing is planned, the procedure details should be explained to the patient, including what he/she is expected to hear and feel, inside the O.R.

✔️Get a brief description of the seizures and any prodromal symptoms 

✔️Continue anti epileptics through the morning of surgery

✔️Antiepileptics can reduce duration of action of NMBAs

✔️Usually a preoperative WADA test or fMRI would have been done, to check, whether the side of proposed surgery has any cerebral dominance or speech function 

✔️Abnormal LFTs can be expected with long term Valproate or Carbamazepine therapy

✔️WHAT THE COMMON AEDs DO?

✔️Phenytoin and Phenobarbitone: Reduce Hematocrit

Carbamazepine, Valproate,Ethosuximide and Primidone : Reduce platelet count

Carbamazepine and Primidone: Reduce WBC count

✔️If a difficult intubation is anticipated ( for e.g. After fixation of stereotactic frame ), an awake fibreoptic intubation can be considered 

✔️Moderate Sedation, if required can be achieved with Propofol 25-75 ug/kg/min plus Remifentanil 0.02-0.05 ug/kg/min OR Dexmedetomidine 1ug/kg/min over 10 minutes followed by 0.2-0.7 ug/kg/min

✔️Anticipated Surgical duration: 3 hours

✔️EBL: 250-500 ml ; blood transfusions are seldom needed

✔️Pain score 2-4

✔️If an Asleep-Awake-Asleep technique is used:

GA  continued for positioning, craniotomy and till the exposure of the surgical area. Then patient is allowed to awaken, to monitor neurological function during brain stimulation ( LMA removed OR  if ETT, it is removed over a tube exchanger). When seizure area, is fully delineated, GA is reinstituted.

AETIOLOGIES AND ASSOCIATED CONDITIONS IN PATIENTS COMING FOR EPILEPSY SURGERY

AETIOLOGIES 

〰〰〰〰〰

🏷Idiopathic (Mesial Temporal Sclerosis)

🏷Infectious (Brain Abcess, Encephalitis)

🏷Traumatic (glial scar)

🏷Vascular (AVM, Infarct)

🏷Neoplastic (glioma, hamartoma, ganglioglioma)

🏷Congenital (Cortical dysplasia)

ASSOCIATED CONDITIONS 

〰〰〰〰〰〰〰〰〰〰

🏷Tuberous Sclerosis

🏷Sturge Weber Syndrome 

🏷Infantile Hemiplegia

🏷Encephalitis

EPILEPSY SURGERY: OTHER APPROACHES

💈1) Frontal/temporal or occipital craniotomy for resection of a structural epileptogenic focus e.g. Tumour or AVM

🔺This may use stereotaxic localisation (by using a stereotaxic headframe, which may affect the method of intubation)

💈2) Diagnostic placement of surface or depth electrodes

 🔺Mostly only burr holes outlining the future craniotomy flap are used

🔺After placement, the electrodes are externalised and postoperatively patient’s naturally occurring seizures are recorded in conjunction with video monitoring, to register the clinical presentation, with the onset of seizure activity. This recording period may last for several days.

🔺This will be followed by resection of the epileptic focus, on another date.

💈3) Selective amygdalo-hippocampectomy

🔺Here, a cortical incision is made in the anterior temporal lobe and amygdala & hippocampus are resected

💂ATRIAL NATRIURETIC FACTOR💂

💧26 AA peptide hormone 

💧synthesised from a prohormone in atrial secretory granules released in response to atrial stretch /  wall tension 

💧plasma half life, t ½ β  ~ 3 mins 

💧maximal natriuresis is less than that seen with frusemide

💧however ANF is ~ 100 times as potent 

💧receptors are concentrated in cortical  glomeruli 

💧the postulated second messenger is cGMP ? 

💧there is no direct effect upon Na +  transport, or the Na + /K +-ATPase 

💧neither amiloride nor prostaglandin inhibitors have an effect upon its actions 

💧ANF effects include

🎯systemic vasodilatation ( mostly venodilation--> transient hypotension, decreases preload

🎯increases salt delivery to distal tubule

🎯decreases plasma renin 

🎯decreases plasma aldosterone 

🎯increases urinary excretion of Na, K, Ca, Mg, Phosphate, Chloride

🎯increases urine volume

EPILEPSY SURGERY- VARIANT APPROACHES🙇🙇🏻🙇🏼🙇🏾: CORPUS CALLOSOTOMY

✔️Suited for patients with atonic or partial seizures with secondary generalisation 

✔️Either the anterior 2/3rd or the entire corpus callosum is divided in the midline

✔️Uses a bifrontal paramedian scalp incision and elevation of the free bone flap, adjacent to the midline in the region of the coronal suture

✔️Injury to the sagittal sinus can result in massive VAE or haemorrhage 

✔️Preserve the numerous bridging veins across the interhemispheric fissure; otherwise, can result in venous congestion and possible infarction 

✔️Right cerebral hemisphere is gently retracted from the falx: this will expose the paired anterior cerebral arteries and corpus callosum

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EPILEPSY SURGERY: SPECIFIC PROCEDURES & HIGHLIGHTS : TEMPORAL LOBECTOMY

✔️ Head turned 90* and held with pins

✔️ Most commonly a "question mark" temporal incision

✔️ a flap based on temporalis muscle elevated

✔️ a subtemporal craniectomy allows visualisation of entire anterior temporal lobe

✔️ anterior 6-6.5 cms of temporal lobe exposed

✔️ surface or depth electrocorticography employed

✔️ map the lesion

✔️ amygdala, hippocampus/ anterior temporal lobe removed 

✔️ Temporal lobectomy involves resection of both lateral and medial (uncus, hippocampal formation etc) temporal structures, mostly under an operating microscope

✔️ Complications: Injury to brainstem, 3rd and 4th cranial nerves , Middle or Posterior Cerebral arteries

✔️ closure of dura, bone flap and scalp concludes the surgery

#epilepsy , #seizures ,#neurosurgery , #EpilepsySurgery , #NeuroAnaesthesia ,#NeuroAnesthesia , #speech ,#wadatest

☁️EPILEPSY SURGERY: BASIC FACTS

☄Most beneficial in partial seizures secondary to a structural lesion

☄For determining the cerebral dominance and hence the location of speech , a WADA test (intracarotid injection of anesthetic to localize language function ; hence invasive) or recently functional MRI mapping (non invasive) of speech centres are done preoperatively 

☄Simultaneous recordings of video EEG and MRI or PET scans can show the epileptogenic focus

☄Temporal lobe surgery may involve:

✔️removal of only the structural lesion & associated epileptogenic cortex

✔️cortical resection alone

✔️excision of amygdala and hippocampus 

✔️removal of the entire anterior temporal lobe (extent of posterior resection dependent on dominance)

✔️depending on the local protocol, intraoperative Electro Corticogram (ECoG) may be used; anesthesia has to be modified accordingly

✔️if speech centre has to be located intraoperatively, an awake craniotomy is required

✔️ So depending on the surgical plan, choice of anesthesia varies

ADVERSE EFFECTS OF UNDER TREATED SEVERE ACUTE PAIN

(Reference: Pamela E. Macintyre,Stephan A. Schug. ACUTE PAIN MANAGEMENT; A PRACTICAL GUIDE)

👹Tachycardia, hypertension

👹increased myocardial oxygen consumption, myocardial ischemia

👹 Decreased lung volumes, atelectasis, decreased cough, sputum retention, infection, hypoxemia

👹Decreased gastric and bowel motility 

👹Urinary retention 

👹Increased catabolic hormones: glucagon, growth hormone, vasopressin, aldosterone, renin, and angiotensin 

👹Reduced anabolic hormones: insulin, testosterone 

👹Catabolism leads to hyperglycemia, increased protein breakdown and negative nitrogen balance; ➡️impaired wound healing and muscle wasting 

👹 Muscle spasm, immobility (increasing risk of deep-vein thrombosis-->pulmonary embolism) and muscle wasting 

👹 Chronic (persistent) pain due to central sensitization 

👹 Anxiety, fear, helplessness, sleep deprivation—leading to increased pain and potential long-term psychological effects