Pages

Showing posts with label neuroanaesthesia. Show all posts
Showing posts with label neuroanaesthesia. Show all posts

Friday, August 19, 2016

HOW EVOKED POTENTIALS BEHAVE , WHEN BRAIN SUFFERS FROM ISCHEMIA ❓


🕶Cerebral ischemia slows neurotransmission and neuronal energy metabolism, resulting in decreased amplitude and increased latency of specific peaks. 

🕶For SSEPs, a 50% reduction in amplitude and/or a 10% increase in latency [changes in the central conduction times, namely, the interpeak latencies between the N14 and N20 peaks] of SSEP signals from the baseline are generally accepted to be a significant change 

🕶A 50% reduction on SEP amplitude has been shown to occur when cerebral blood flow decreases below 14 mL/100 g/min 

🕶MEP have less well-defined warning criteria as compared to SSEPs; however, increased stimulus thresholds and/or decreased MEP amplitudes in relation to dramatic events (i.e., clip application) are indicative of pending neurologic insult. 

🕶For BAEP, an increase in latency of more than 1 msec, particularly in wave V, is considered to be clinically significant. 

🕶Unlike EEG monitoring the evoked potential tests can detect subcortical functional status by way of perforating branches such as the anterior choroidal and medial striate arteries 

Reference: Anesthesiology Research and Practice Volume 2014, Article ID 595837, Controversies in the Anesthetic Management of Intraoperative Rupture of Intracranial Aneurysm, Tumul Chowdhury, Andrea Petropolis,Marshall Wilkinson, Bernhard Schaller  Nora Sandu and Ronald B. Cappellani

Wednesday, March 9, 2016

MECHANISMS THROUGH WHICH HYPERGLYCEMIA WORSENS NEUROLOGICAL OUTCOME


✔️Hyperosmolality 
✔️Lactic acidosis
✔️Alterations in neuronal pH
✔️Increase in excitatory Amino Acids

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

Thursday, February 4, 2016

Systemic complications of aneurysmal subarachnoid hemorrhage



🔺Hypovolemia
🔺Hyponatremia
🔺Hypokalemia
🔺Hypocalcemia
🔺Electrocardiographic abnormalities
🔺Pulmonary edema
🔺Pneumonia
🔺Pulmonary embolus
🔺Hepatic dysfunction
🔺Renal dysfunction
🔺Thrombocytopenia
🔺Gastrointestinal bleeding


Friday, January 29, 2016

INTRACRANIAL ANEURYSMS : GENETICS AND ASSOCIATED DISEASES



Of patients who have SAH from ruptured aneurysm, 5% to 10% will have one or more first-order relatives who have also had a ruptured aneurysm. 

The inheritance is probably dominant with variable penetrance. 

Conditions associated with intracranial aneurysms include 〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰〰

🏷polycystic kidney disease (5% of aneurysms series, 33% of polycystic kidney series)

🏷coarctation of the aorta (1% of aneurysm patients, 5% of coarctation patients, all of whom are hypertensive)

🏷sickle cell disease

🏷drug abuse (cocaine: generalized vasoconstriction and hypertension; intravenous use: mycotic aneurysms)

🏷hypertension (30% to 40% of patients with SAH). 

Rarer associations 
〰〰〰〰〰〰〰
🏷fibromuscular dysplasia

🏷Marfan's syndrome

🏷tuberous sclerosis

🏷Ehlers-Danlos syndrome

🏷hereditary hemorrhagic telangiectasia

🏷moyamoya disease

🏷pseudoxanthoma elasticum. 

🏷Choriocarcinoma 

🏷cardiac myxomas 


Ref: Handbook of Neuroanesthesia, 4th Edition, p:144

Wednesday, January 20, 2016

Predisposing factors for rebleeding after Aneurysmal SAH


🔹Large volume of blood in the subarachnoid space from the initial SAH

🔹Poor neurologic status owing to the devastation caused by the initial SAH

🔹Short interval from the initial hemorrhage

🔹Female gender: women rebleed twice as frequently as men

🔹Older age and poor general medical condition

🔹Systemic hypertension: the risk of rebleeding is directly related to the patient's systolic blood pressure

🔹Multiple previous episodes of rebleeding that increase the likelihood of subsequent rupture and death

🔹Presence of either an intracerebral or intraventricular hematoma

🔹Abnormal clotting parameters

🔹Posterior circulation aneurysms

Ref: Philippa Newfield, Audrée A. Bendo, Handbook of Neuroanesthesia, 4th Edition, 2007 Lippincott Williams & Wilkins


Monday, January 18, 2016

ANTERIOR AND POSTERIOR APPROACHES TO CERVICAL SPINE / SAFE Anesthesiologist Series [Surgical Aspects For Empowering Anesthesiologist]



ANTERIOR APPROACH TO CERVICAL SPINE
➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖

✔️ADVANTAGES

Easy access to disc
Little pain
Evacuate disc
Fusion by plate or graft

✖️DISADVANTAGES 

Multiple levels difficult 
May require fusion if unstable
Loss of mobility 
Risk of injury to adjacent structures

POSTERIOR APPROACH TO CERVICAL SPINE
➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖➖

✔️ADVANTAGES

Access to multiple levels
Direct visualisation of root
Fusion is usually not required

✖️DISADVANTAGES 

Risk of instability 
Poor access to disc space
Poor access to osteophytes
Higher risk of cord injury
Painful procedure


Ref: Bailey & Love’s Short Practice of Surgery, 24/e

Saturday, January 16, 2016

💹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)

Thursday, January 14, 2016

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

Monday, January 11, 2016

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.