JOURNRL OF millTRRV PHflRMflCO-MEDICINE N°7-!014
CASE REPORT: LOSS OF CONSCIOUSNESS AND APNOEA FOLLOWED BY SPINAL ANESTHESIA WITH LOW DOSE BUPIVACAINE IN THE ELDERLY
Nguyen Trung Kien*
SUMMARY
After spinal anesthesia with low dose buplvacaine, complication of loss of consciousness is very rare. The cause for this condition In some cases mmalns to be unclear We mport the eklerly patient who lost consciousness and apnoea within 2.5 hours alter subarachnoid block with low dose buplvacaine and fentanyl at 103 Hospital The patient's blood pressure decreased suddenly befom toss of consciousness. She was discharged 6 days after Incident and completely recon/emd.
' Key words: Loss of consciousness; Apnoea; Spinal anesthesia. Low-dose buplvacaine; Elderly
INTRODUCTION
Spinal anaesthesia (SA) can safely provide excellent operating conditions for surgery below ttie umbilicus. There are many advantages of SA over general anesthesia such as reducing metabolic stress response to surgery and anesthesia:
decreasing the incidence of venous thromboembolic complications; endotracheal intubation is avoided [1]... However, there are potential complications that the anesthetist must l<now. Because SA will block sympathetic nerves, resulting in vasodilatation, which may cause a large fall in the patient's blood pressure and a decrease in heart rate, especially, in the elderly patients. A high spinal block may make the patient unconscious and stop breathing [5]. We report the elderly patient who lost consciousness and apnoea within 2.5 hours after spinal anesthesia with low dose buplvacaine and fentanyl.
CASE REPORT
A 80-year-old female patient, 158 cm, 82 kg with history of Paklnson' disease for ten years who was diagnosed bleeding in anal canal, required an emergency surgery for hemostasis. ECG was normal with sinus rhythm; blood pressure 145/80 mmHg;
respiratory rate was 15 per minutes.
Blood test: Red blood cell 4.22 x lO'/L, hemoglobin 136 g/L, hematocrit 0.46 L/L, platelet 199 G/L, albumin 44 g/L; protein 68 g/L; creatinine 145 pmol/l, urea 5.6 mmol/l; glucose level 5.4 mmol/l; GOT 38 U/L; GPT 36 U/L. Plasma electrolytes were normal (sodium 146 mmot/l; potassium 3.4 mmol/l). Abdominal ultrasound and chest X-ray were normal.
- Intravenous canulation was done with 18G needle, preloading was done with ringer ladat 10 ml/kg; momitor ECG, heart rate, oxygen saturation (SPO2), blood pressure in 2.5 minutes' interval; oxygen was given through face mask at rate 3 L.min'V
' 103 Hospital
Conesponding author: Nguyen Trung Kien ([email protected])
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JOURNRL OF IVIILITRR¥ PHRRmRCO-mCDIClNe N°7-20I4
- Subarachnoid block was performed 67 beats min '. sinus ECG, 60% of Sp02.
at L3-L4 intervertebral space in lateral Ventilation through face mask was done position with 5 mg of buplvacaine and 20
pg of fentanyl. Patient was immediatelly turned supine and horizontal plane.
- A T6 sensory level block was achieved in 2.5 minutes. Bromage score was 3 and oxygen saturation was 100% at that time.
No drug was administered and patient was alert and can communicate normally with anesthetist. Two hands was tremored as the feature of Pakinson' disease. Blood pressure fell down to 86/62 mmHg level in 10 minutes and 10 mg of ephedrin was intravenous administered.
- After 10 minutes' injection of intrathecal drug, patient suddently stopped communication and the hand did not tremor any more.
She did not evep respond to verbal commands and deep pain stimulation.
There was no uprolling of eyes or frothing.
The pupils' zise and shape were norma*
and reactive to light. There was no complains about chest pain or weakness of the upper limbs immediately before losing consciousness. At that time, blood pressure was 123/71 mmHg, heart rate
at rate 20 timesmin'. SpOj reached 100/o after 3 minutes' ventilation. Although haemodynamics and heart rate and SpO, gained normal levels, she was still unconscious and no spontaneous breathing.
Endotracheal tube was intubated easily without muscle relaxant and larynx reflex was not seen, too. 0.4 mg of naloxone was slowly intravenous administered.
- After 45 minutes' subarachnoid blocl<, blood pressure reached highest level of 180 - 210/98 -105 mmHg. However, there was no awake signs or larynx reflexs or sweat or tears. 1 mg of nicardipin was slowly intravenous injected, haemodynamic returned to around level of 135 -140/76 - 81 mmHg. Vital signs were monitored by Nihon Kohden.
- Two and half an hour after spinal anesthesia, the patient had larynx reflex and responded to verbal commands as well as pain stimulation. Endotracheal was extubated and the patient completely recovered after 2.5 hours. She was discharged after 6 days of treatments.
TaWe 1: Vital signs after subarachnoid block.
POST SUBARACHNOID
' BLOCK (mm) 1 2.5
6 6 7.6
10 12 15 20
SYSTOLIC/DIASTOLIC PRESSURE (mmHg)
146/82 128/72 110/62 121/66 86/62 123//1 132/76 135/72 140/75
HEART RATE (mm'') 82 80 76 66 58 67 75 76 78
SPOj
(%)
100 100 100 100 96 60 98 99 100
NOTES
2 5 5 ! : i ^ ! ! : ! ! L ' ! l ! : ? W a c e mask of 31 min-' Sensory level reached at TR Surgery started
— — — ^
Slowly injectin^joJ^^^f^^fj^^T; 1
~~~~-— '
Ventilation through facp
of oxygen "mask with 100%
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JOUANRL OF MILITRRV PHRRMRCO-MCDICINE N°7-2014
30 40 45
60 160
138/77 180/98
^ 210/106
140/81 135/76
82 86 87
85 88
100 100 100
100 100
Endotracheal was intubated No larynx reflex, no tear and sweat Pupils'size was 3 mm wide.
Reactive to light (+) Slowly Iniectino 1 mo of nicardloin
Recoved
DISCUSSION
Some conditions may be contributive factors. Firstly, the patient had a blood sugar concentration of 5.4 mmol.lltre"^
and that was normal and was not the reason for loss of consciousness. Furthemiore, she had no history of epileptic seizure and this cause may be eliminated. The nonnal ECG preoperative and intraoperative period indicated that the event could not explained by arrhythmias.
It's certain that loss of consciousness could not be attributed to any intravenous sedative or narcotic drugs being given inadvertently before spinal anesthesia technique. According to David Pescod [3], the addition of opioid improves the quality and duration of analgesia but also increases fisk. It is safe to add 10 to 20 pg of fentanyl intrathecally. Only when receiving a single spinal dose of morphine (0.1 to 0.3 mg), are patients at risk of early (within 2 hours) and late (within 6 to 12 hours) respiratory depression. Opioids produce intense visceral analgesia and may prolong sensory blockade without affecting motor or sympathetic function. The major sites of action are opiate receptors within the second and third laminae of the substantia gelatinosa in the dorsal horn of the spinal cord.
Lipophilic agents such as fentanyl have a much more localized effect than the hydrophitic agents such as the hydrophilic opioid morphine. Fentanyl has a rapid onset action and effective duration more
than 6 hours (morphine lasts 6 - 24 hours) [1]. Side efects indude respiratory depression (which may occur late with hydrophilic agents), nausea, vomiting, pruritus and urinary retention. However, only 20 pg fentanyl (combined with 5 mg buplvacaine heavy) was given intrathecally. In addition, apnoea occured at the same time with loss of consciousness and loss tremor of the hands. The patient was also administered intravenous slowly with 0.2 mg of naloxon, an opioid antagonist, but there was no signs of recovery. It was the reason that respiratory center was not Inhibited,
Intra-operative troke may be attributed to that event because of losing sudden mnsciousness. Blood pressure significantly increased, systolic pressure reached 180 to 210 mmHg in 45 min after SA (table 1), These symtoms happened without any awake signs (sweat, tearing, cough reflex).
However, both of her pupils were about 3 mm wide and still reactive to light. A CT scan done after surgery was normal, this indicated that there was no space occupying lesion intracraniatly to account for the loss of consciousness intra-operative time
According to Fateh Singh Bhati [4], loss of consciousness is usually due to severe hypotension from a high spinal block with large dose of local anesthetic The signs of cephalad extension of the block are usually not as clean as with an immediate total spinal block, and patients may complain about dyspnoea, weakness of the amis or dysarthria. There may be
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JOURNRl OF MILITRRV PHRRMRCO.MCDICINe N°7-2014 no warning before unconsciousness suddenly sometimes occurs after the block has been inserted [2]. Our patient loss consciousness and apnoea occurred 10 minutes after spinal anesthesia in the present of remarkable haemodynamic stability. However, her blood pressure (86/62 mmHg) decreased sharply at 7.5 min after spinal anesthesia {table 1). It fell down approximately 4 1 % compared with baseline value. As a result, cerebral blood flow deceased suddenly and the patient could have lost consciousness as a psychogenic response to distress at that time. However, patient's blood pressure returned to normal immediately after slowly Intravenous Injected by 10 mg ephedrin and loading fluid.
Spinal anesthesia can cause hypotension, which depends on the dose used. According to Barash [1], drug dose and volume appear to be relatively unimportant in predicting the spread of hyperbaric local anesthetic solutions injected in the horizontal position.
Increasing the dose and volume of hyperbaric tetracaine, while holding concentration constant, does not affect block height when doses between 7.5 and 15 mg are used. However, the dosage for Vietnamese people may be lower than the same sensory level. Methods commonly used to prevent or treat hypotension, including fluid preloading, the use of hyperbaric buplvacaine, positioning to relieve aortocaval compression and vasopressor therapy. In the study of Pekka Tarkkila [6], he described hypotension during spinal anesthesia principally results from the preganglionic sympathetic blockade.
Systemic vascular resistance decreases as a result of a reduction in sympathetic tone of the arterial circulation. This leads to peripheral arterial vasodilatation, the extent of which depends on the number of spinal segments involved.
In our patient, hypotensive effects of spinal anesthesia may be exacerbated by Parkinson' disease, caused by neurodegenerative disorder which leads to progressive detenoration of motor function due to loss of dopamine-producing brain cells. TherefoiE, chronic dopaminergic therapy was also a crucial reason for vasodilation and systemic hypotension made systolic blood pressure deaease sharply In this case.
In conclusion, we have described loss of consciousness after spinal anesthesia.
Losing consciousness occurred after blood pressure falls in a short time. It Is speculated that hight spinal block may be attributed to be low dose buplvacaine in the elderly patient. Furthermore, unconsciousness may be exacerbated by Parkinson'dlsease and drug for treatment.
REFERENCES
1. Barash, Paul G, Cullen, Bruce F, Stoelting, Robert K Epidural ans spinal anesthesia.
Clinical Anesthesia, 5th Edition, Lippincott Williams & Wilkins. 2007, pp.700-705.
2. Chan Y. K, Goplnathan R., Rajendram R. Loss of consciousness following spinal anesthesia for caesarean section, Bristish Joumal of Anaesthesia. 2000, 86 (3), pp.474-476.
3 David Pesood. Regbnalanesthesa [Developing anesthesia texltxwks, www.developinganaesthesia.o(g.
2007, pp.125-135,
4. Fateh Singh Bhati, Vinod Kumar Vijayveigia, Vijay Laxmi Jain. Loss of consciousness following spinal anesthesia for caesarean section. Indian Journal of Anaesttiesia. 2004, pp.57-58.
5. Lamacmft G. Complications associated with regional anaesthesia for Caesarean section.
Southern African Journal of Anaesthesia &
Analgesia. 2004 pp.15-20.
8. Pekka Tartdrlla. Complications associated with spinal anesthesia Complications of regional anesthesia. Springer Science+Business Media LLC, USA. 2007, pp.149-166.
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