Update: Adenosine-induced cardiac standstill with hypotension

Several flow-arrest techniques have been introduced for the treatment of complex aneurysms that cannot be treated with conventional clipping or endovascular coil embolization. Adenosine-induced transient asystole is an alternative method of flow arrest.

Adenosine-induced flow arrest briefly reduces cerebral perfusion pressure and reduces the turgor of the aneurysm, thereby facilitating the clip ligation in complex aneurysms. Periods of flow arrest have to be carefully coordinated with the surgeon such that necessary working time is available for aneurysm dissection and clip placement. Adenosine-induced transient asystole is safe and efficacious when administered at an average of 0.3 to 0.4 mg/kg IBW in combination with remifentanil/low-dose volatile anesthetic with propofol. The adenosine dose will achieve approximately 45 seconds of controlled systemic hypotension and a bloodless surgical field. Adenosine offers the advantage of easy applicability in different situations without advanced preparation or complex logistical coordination with anesthesiology and cardiovascular surgery. This technique also allows the surgeon to have the maximum amount of space available to manipulate the aneurysm and place the clips, as no temporary clips are in the field of view. Also, temporary clips only decrease flow from the clipped inflow, whereas adenosine produces a more global hypotension and therefore often a better collapse of the aneurysm 1).
Adenosine-induced asystole for cerebral aneurysms surgery was first described by Groff et al. 2) in 1999 in posterior circulation aneurysms.
It is an easily applied technique in a variety of clinical situations. Its use requires minimal advanced preparation and no complex logistical coordination with other subspecialties. However, patient-specific dose-response relationships must be determined by exposure, so the relationship may not be known in an emergent situation. Persistent hypotension is a potentially major complication. Rapid ventricular pacing (RVP) has recently been reintroduced into cerebrovascular surgery. It is more predictable than adenosine in response time and, thus, can be used during unanticipated complications, such as aneurysmal rupture. It also induces a shorter period of hypotension compared with adenosine. However, RVP is more invasive and more complex from an anesthesia standpoint. Vascular neurosurgeons should be familiar with these techniques and know their applications and limitations 3).

Case series

2017

The aim of a study is to report the experience in the use of adenosine in aneurysm clipping and arteriovenous malformation (AVM) resection and review the literature. The records of all patients who had adenosine-assisted clipping of intracranial aneurysms and AVM resections between November 2015 and December 2016 were extracted from prospectively maintained database. The following data were collected: patient demographics, comorbidities, size and location of the aneurysms or AVM, number of boluses and total dose of adenosine administered, duration of cardiac standstill and hypotension (systolic blood pressure < 60 mmHg), intraoperative and postoperative complications and outcome scores at discharge. Literature search on Embase and PubMed for the terms “adenosine and clipping”, “adenosine and aneurysm” and “adenosine and AVM” was performed. Eight aneurysms and two AVMs were identified. While both AVMs were elective procedures, half of the aneurysm clippings were on urgent basis.
Al-Mousa et al. used adenosine safely with spontaneous return of rhythm in all cases. Temporary clips to the parent artery were applied for brief periods in 2 patients who had pre-adenosine intraoperative rupture. They did not observe any immediate or late adverse events related to administration of adenosine.
In a review, a total of ten case series and four case reports were identified. There were no reports on the use of adenosine in AVM resection. Transient adenosine-induced asystole is a safe and effective technique in facilitating surgical treatment of complex aneurysms and AVMs. In addition, adenosine use reduces the need, duration, and associated complications of temporary clip applications to parent arteries 4).

2015

A total of 22 aneurysms in 22 different patients that underwent adenosine-induced transient asystole during aneurismal neck clipping within the past 4 years were retrospectively reviewed. Adenosine was administrated intravenously in a test-incremental manner (starting with 6-12 mg and then giving additional doses as needed) in 11 patients and in an estimated manner (pre-calculated as 0.3-0.4 mg/kg) in 11 patients.
Overall, the study consisted of 18 unruptured saccular aneurysms, three ruptured saccular aneurysms, and a ruptured pseudoaneurysm. Adenosine-induced transient asystole was used in cases of temporary clipping inability, wide necked aneurysm, deep-seated aneurysm, or a thin aneurysm wall. The number of administrations, dose (mg/kg in ideal body weight) and duration of asystole were 1-4 (mean, 2.3) times, 0.08-1.27 (mean, 0.36) mg/kg and 0-30 (mean 13) seconds in the test-incremental manner and 1-2 (mean, 1.09) times, 0.24-0.42 (mean, 0.34) mg/kg and 13-41 (mean, 24) seconds in the estimated manner, respectively. There was a linear relationship between the dose and the duration of asystole. Twenty out of 22 aneurysms were clipped successfully with adenosine-induced transient asystole. However, in the other two cases, additional suction decompression was required for the final clipping. Adenosine-related cardiologic complications occurred in two cases of self-limited atrial fibrillation during restoration of the cardiac rhythm.
In our experience, adenosine-induced transient asystole was safe and helpful for satisfactory clipping of a complicated aneurysm. An estimated dose injection of adenosine was more convenient than the test-incremental method and did not result in serious cardiologic problems 5).

2009

A report describes three children, aged eight to 11 years, with high-flow cerebral arteriovenous malformations who underwent interventional neuroradiological procedures involving glue (N-butyl cyanoacrylate) embolisation under general anaesthesia. The procedure was facilitated by relative hypotension induced by esmolol infusion and intravenous adenosine boluses. To allow controlled deposition of N-butyl cyanoacrylate into the arteriovenous malformations, glue injection was synchronised with the onset of adenosine-induced brief cardiac standstill. This resulted in satisfactory obliteration of the arteriovenous malformations nidus in all cases. The haemodynamic modulations, including the adenosine-induced brief cardiac standstill, was noted to not affect the BIS values in our patients. All patients had satisfactory obliteration of their arteriovenous malformations and had good neurological outcomes at one-year follow-up 6).
1)

Britz GW. Adenosine-induced transient asystole. Methodist Debakey Cardiovasc J. 2014 Oct-Dec;10(4):220-3. doi: 10.14797/mdcj-10-4-220. Review. PubMed PMID: 25624976; PubMed Central PMCID: PMC4300060.
2)

Groff MW, Adams DC, Kahn RA, Kumbar UM, Yang BY, Bederson JB. Adenosine-induced transient asystole for management of a basilar artery aneurysm. Case report. J Neurosurg. 1999 Oct;91(4):687-90. PubMed PMID: 10507394.
3)

Rangel-Castilla L, Russin JJ, Britz GW, Spetzler RF. Update on transient cardiac standstill in cerebrovascular surgery. Neurosurg Rev. 2015 Oct;38(4):595-602. doi: 10.1007/s10143-015-0637-z. Epub 2015 May 1. PubMed PMID: 25931209.
4)

Al-Mousa A, Bose G, Hunt K, Toma AK. Adenosine-assisted neurovascular surgery: initial case series and review of literature. Neurosurg Rev. 2017 Jul 22. doi: 10.1007/s10143-017-0883-3. [Epub ahead of print] Review. PubMed PMID: 28735438.
5)

Lee SH, Kwun BD, Kim JU, Choi JH, Ahn JS, Park W, Yun JH. Adenosine-induced transient asystole during intracranial aneurysm surgery: indications, dosing, efficacy, and risks. Acta Neurochir (Wien). 2015 Nov;157(11):1879-86; discussion 1886. doi: 10.1007/s00701-015-2581-7. Epub 2015 Sep 18. PubMed PMID: 26385113.
6)

Puri GD, Sen I, Bapuraj JR. Adenosine-induced cardiac standstill to facilitate endovascular embolisation of cerebral arteriovenous malformations in children. Anaesth Intensive Care. 2009 Jul;37(4):619-23. PubMed PMID: 19681422.

Intracranial hypotension: clinical presentation, imaging findings, and imaging-guided therapy

Intracranial hypotension is a condition in which there is negative pressure within the brain cavity.

Etiology

see Spontaneous intracranial hypotension
Cerebrospinal fluid leak from the spinal canal:
A leak following a lumbar puncture (spinal tap).
A defect in the dura
Sometimes following exertion such as swinging a golf club.
A congenital weakness.
Following spinal surgery.
Following spinal trauma.
Following a shunt procedure for hydrocephalus.
Lumboperitoneal shunt.
Ventriculoperitoneal shunt with a low pressure valve.
In some cases, spinal CSF leaks can lead to a descent of the cerebellar tonsils into the spinal canal, similar to a Chiari malformation.
Large spinal dural defects can lead to herniation of the spinal cord into the defect.

Symptoms

The classic symptom is severe headache when upright, which is relieved when lying flat.
Other symptoms can include nausea, vomiting, double vision and difficulty with concentration.
The typical clinical manifestation – orthostatic headache – may be masqueraded by atypical clinical findings, including coma, frontotemporal dementia, leptomeningeal hemosiderosis-associated symptoms, and others.

Diagnosis

Diagnosis is usually suspected based on the postural dependency of the headache, although in many cases the diagnosis of intracranial hypotension is not considered for some time.
A contrast-enhanced brain magnetic response imaging (MRI) scan typically shows thickened and brightly enhancing meninges (pachymeningeal enhancement). Other findings include descent of the thalamus and cerebellar tonsils.
MRI signs are highly specific, but the imaging strategy to search for spinal cerebrospinal fluid leaks (none, computed tomography myelography, magnetic resonance myelography with gadolinium, digital subtraction myelography) is a matter of debate 1).
Continuous intracranial pressure monitoring is definitive for documenting abnormally negative intracranial pressures.
The identification of the site of CSF leak in the spinal canal can be very challenging. In some cases, the site cannot be identified. Methods include:
Dynamic myelography with fluoroscopy and computed tomography (CT).
Radioisotope cisternography.
Spinal MRI.

Treatment

If the site of the spinal CSF leak can be identified, then options include:
Epidural blood patch, performed by an anesthesiologist pain management specialist.
Surgical repair of the defect.
Over-draining CSF shunts are managed by replacing the valve with one that drains less.
Lumboperitoneal shunts may have to be removed or ligated.

Outcome

If the cause of the intracranial hypotension can be identified, the outcome following treatment is typically excellent.
1) Urbach H. Intracranial hypotension: clinical presentation, imaging findings, and imaging-guided therapy. Curr Opin Neurol. 2014 Aug;27(4):414-24. doi: 10.1097/WCO.0000000000000105. PubMed PMID: 24978633.
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