Positioning of the anesthetized patient and cerebral perfusion: foreseeable catastrophes

EDITORIAL

Positioning of the anesthetized patient and cerebral perfusion: foreseeable catastrophes

Recently, Cullen and Kirby ¹ reported the case of a patient undergoing arthroscopy of the shoulder under general anesthesia, who developed a catastrophic complication leading to a permanent vegetative state. The patient was 47 years old, healthy, with preoperative blood pressure of 125 ´ 83 mmHg. Pre-anesthetic medication consisted of the intramuscular administration of 50 mg of meperidine, 40 mg of hydroxyzine and 0.2 mg of glycopyrrolate. Anesthetic induction was achieved with the intravenous administration of 200 mg of propofol, 100 mg of succinylcholine and 30 mg of lidocaine followed by endotracheal intubation. As the patient developed hypertension, 50 mg of labetalol were administered intravenously. Anesthesia was maintained with 2.0% isoflurane, 60.0% nitrous oxide and oxygen. The patient was placed in the beach chair position for the procedure. Twenty minutes after the beginning of the surgery the blood pressure decreased to 100 ´ 60 mmHg and then to 80 to 90 mmHg (systolic) remaining at this level until the end of the procedure. SatO₂ remained at 100% and P_ETCO₂ approximately 30 mmHg during the procedure.

When the patient arrived at the recovery room, she was unconscious but her blood pressure was 113 ´ 60 mmHg and she remained intubated. Intravenous naloxone, 0.1 mg, was administered without response or movement of the extremities. Another dose of 0.1 mg of naloxone was administered 35 minutes after arrival to the recovery room, but the patient did not respond. Three more doses of naloxone and two of physostigmine were administered unsuccessfully. Tracheal intubation was maintained with good oxygenation. The patient was unresponsive to verbal commands and to painful stimuli and deep tendon reflexes were diminished bilaterally. Neurological evaluation suggested a diencephalic syndrome, probably cerebral infarction.

At first, axial CT of the head was normal, but on the 5^th postoperative day it showed cerebral edema and occlusion of the cistern. One week after the procedure, the MRI showed changes in both brain hemispheres suggestive of cortical infarctions in the anterior and temporal lobes without edema or herniation. There was no indication of intracranial bleeding. After two weeks she presented a score of 3 on the Glasgow scale. She presented corneal reflexes, hyperreflexia, increased muscle tone and no response to painful stimuli in all four extremities. A diagnosis of permanent vegetative state was made.

This dramatic case illustrates the importance of patient positioning for surgical procedures. The beach chair position allows the patient to remain in the sitting position in angle that vary from 30° to 90° above the horizontal plane, which is ideal for arthroscopic surgeries of the shoulder avoiding changes in the intra-articular anatomy and making the access easier for the surgeon, which does not happen with the lateral decubitus.

Nonetheless, important changes occur when the patient is in the sitting position, notably a reduction in the mean arterial pressure (MAP), central venous pressure, systolic volume, cardiac output and PaO₂². In the non-anesthetized individual, those changes are compensated by an increase in systemic vascular resistance, which can vary from 30% to 60%³. However, this response is blocked by the vasodilation caused by anesthetics, which can also decrease the cardiac output. Cerebral perfusion pressure (CPP) decreases approximately 15% in the non-anesthetized patient in the sitting position ² and it can decrease even more during anesthesia due to vasodilation and reduction in venous return.

The observations of Enderby ⁴ that there is a reduction of 0.8 mmHg in systolic blood pressure (SBP) for each 1 cm elevation in relation to the heart are classic. Since MAP is directly proportional to SBP, it is obvious that elevation of the head in relation to the heart leads to a reduction of MAP in the intra-cranial territory, which is accentuated during anesthesia due to the reasons mentioned before.

Cerebral perfusion pressure depends directly on the MAP according to the equation:

CPP = MAP - CVP^*

The concept that self-regulatory mechanisms of the cerebral blood flow (CBF) tend to maintain a constant flow when MAP is between 50 and 150 mmHg is also classic ⁵. When MAP is below 50 mmHg, self-regulatory mechanisms do not work and CBF shows a linear and dangerous reduction paralleling the CPP.

In view of those considerations, maintenance of MAP equal or above 50 mmHg has been recognized as the safety threshold in hypotensive anesthesia, which is used to reduce perioperative bleeding ⁶.

Here, two important considerations should be made.

First, in the sitting position MAP in the brain is smaller than the MAP measured at the upper extremity when the patient is supine due to the observations of Enderby mentioned before ⁴. This difference is frequently ignored by the anesthesiologist and can endanger adequate cerebral perfusion during the procedure in the sitting position.

Second, the inferior limit of MAP of 50 mmHg for the mechanism of self-regulation of the CBF has been questioned by some authors ^7,8, who prefer to work with a mean value of 80 mmHg, below which the mechanism would not function properly and CBF would fall especially in patients with poorly controlled hypertension.

In the case discussed here, arterial pressure was monitored by a non-invasive method in the arm, and evidence indicates that the pressure gradient between the arm and the brain was ignored. It is considered that in a patient in the beach chair position there is a 30-cm height difference between the base of the brain (more elevated) and the heart. A blood pressure of 80 ´ 45 mmHg in the arm corresponds to a MAP of 56 mmHg. However, the difference in systolic pressure between the heart and the base of the brain, which is more elevated, is approximately 24 mmHg, meaning that the SBP at the base of the brain is around 56 mmHg and MAP is about 48 mmHg, which does not take into consideration the probable change in diastolic blood pressure. At the cephalad portion of the cerebral cortex, more elevated than the base of the brain, one should add another 10 cm in relation to the level of the heart bringing the SBP to 48 mmHg and MAP to 43 mmHg.

The analysis of those values is consistent with the outcome of this patient. Axial CT of the head on the 5^th postoperative day showed cerebral edema and cisternal occlusion; MRI indicated cortical infarctions in both cerebral hemispheres without evidence of intracranial bleeding. Therefore, the lesions were compatible with intraoperative cerebral hypoperfusion. Besides, the patient was anesthetized with isoflurane, which is known to have vasodilator properties and it certainly hindered a probable increase in systemic vascular resistance to compensate a reduction in MAP and in other circulatory parameters caused by the sitting position.

The lessons of a catastrophic event, such as the one described here, should be taken into consideration in other situations in which the surgery is performed with elevation of the head and the surgeon requests hypotensive anesthetic technique to reduce intraoperative bleeding.

Plastic surgery of the breasts in the sitting position with epidural anesthesia and sedation is one of them. In this case, a reduction in MAP in the brain caused by the elevation of the head will not be compensated by an increase in systemic vascular resistance, since the epidural block (similar to the isoflurane in the case described here) tends to cause vasodilation and reduction in systemic vascular resistance. Under sedation, it is difficult for the anesthesiologist to detect signs of cerebral hypoperfusion during the procedure, and the catastrophe only becomes apparent postoperatively.

The knowledge of physiological changes related with the sitting position, as well as the effects of gravity on blood pressure (and consequently in perfusion) in the brain is fundamental for the prevention of severe neurological complications in surgeries with the patient in this position, regardless of the anesthetic technique used.

Key Words: ANESTHESIA, General; COMPLICATIONS: neurological lesion; positioning

José Roberto Nociti, TSA

Member of the Editorial Council of the Brazilian Journal of Anesthesiology;

Vice-President of the World Federation of Societies of Anesthesiologists;

Responsible for the CET-SBA Santa Casa de Misericórdia de Riberão Preto, SP

REFERENCES

• 01. Cullen DJ, Kirby RR Beach chair position may decrease cerebral perfusion. APSF Newsletter 2007;22:25-27.
• 02. Warner MA, Martin JT Patient Positioning, em: Barash PG, Cullen BF, Stoelting RK Clinical Anesthesia, 4^th Ed, Philadelphia, Lippincott Williams & Wilkins, 2001;639-665.
• 03. Gauer OH, Thron HL Postural Changes in the Circulation, em: Hamilton WF, Dow P Handbook of Physiology. Washington DC, American Physiological Society, 1965; v.3, sect. 2:2409.
• 04. Enderby GEH Postural ischaemia and blood pressure. Lancet, 1954;1:185.
• 05. Michenfelder JD Anesthesia and the Brain. New York, Churchill Livingstone, 1988;94-113.
• 06. Thompson GE, Miller RD, Stevens WC Hypotensive anesthesia for total hip arthroplasty: a study of blood loss and organ function (brain, heart, liver, and kidney). Anesthesiology, 1978; 48:91-96.
• 07. Drummond JC The lower limit of autoregulation: time to revise our thinking? Anesthesiology, 1997;86:1431-1433.
• 08. Drummond JC, Patel PM Neurosurgical Anesthesia, em: Miller RD Anesthesia, 5^th Ed, Philadelphia, Churchill Livingstone, 2000;1895-1933.

*

CVP = Central Venous Pressure; normal @ 8 mmHg

Publication Dates

• Publication in this collection
  17 Jan 2008
• Date of issue
  Feb 2008