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Letters to Editor
Cardiac arrest post tourniquet
release under spinal anesthesia
Sir,
A 60yearold male, ASA Grade 1patient was posted
for implant removal. intramedullary nailing and
bone grafting for nonunion of fracture tibia. He was
operated one year back for fracture of tibia under
subarachanoid block which was uneventful.
His preanaesthetic examination including
investigationswas normal. Patient was shifted with 18 g
intravenous (IV) cannula and started on ringer lactate
solution. He was premedicated with 50 mg of Inj.
Ranitidine and 4 mg of Inj. Ondansetron IV before he
was brought to operating room (OR). Routine monitoring
was established and basal vitals were recorded which
showed heart rate (HR) of 70/min, non-invasive blood
pressure (NIBP) 118/72 mmHg, saturation (SPO2) 97%
on room air and ECG normal sinus rhythm.
Patient was administered Inj. Fentanyl 50 ug IV in OR.
Subarachanoid block was performed in left lateral
position with 25gauge Quincke needle between
L3L4 position. After clear flow of CSF and negative
aspiration of blood, 3.0 ml of Inj. Bupivacaine and25
ug of Inj Fentanyl was injected intrathecally. Sensory
level ofblock of T6 was achieved and 5 lt/min of
oxygen was administered through Hudson mask.
Limb was exsanguinated with an elastic esmarche
bandage and a properly sized tourniquet was
positioned on the operative limb. Pressure was set
to 220 mmHg. But since bloodless surgical field was
not achieved with the above pressure, pressure was
gradually raised to 300 mmHG. Intraoperatively
patient had two episodes of hypotension which was
effectively treated with Inj ephiderine.
Tourniquet was deflated at the end of surgery, after 2
hrs 5 min of inflation time. After 2min of tourniquet
deflation, patient became unresponsive, ECG
showed bradycardia leading to asystole and NIBP
was unrecordable. Immediate cardiopulmonary
resuscitation was started with chest compressions, inj
adrenaline was given IV and intubation and ventilation
with 100% oxygen were performed.
Within 3min, cardiac rhythm reverted back to sinus
rhythm with HR of 48/min which gradually increased to
Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
60/min and NIBP of 80/36mm/Hg. Later patient regained
consciousness and started responding. Immediate
arterial blood gas(ABG) sampling showed pH of 7.1;
serum potassium was 6 meq/lt which was corrected by
sodium bicarbonate and calcium gluconate.
After 30 min, he was shifted to intensive care unit
(ICU) and was continued with ventilation and
IV fluids. His vital parameters including ECG,
echocardiography; cardiac enzymes, lower limb
doppler and CBC was normal. He was ventilated
overnight and extubated next day. His repeat serum
electrolytes and ABG in the morning were normal
and later he was shifted to ward.
Complications like sudden cardiac arrest, pulmonary
embolism, metabolic derangements, neurological
dysfunction have been reported in the literature
after tourniquet use.[1] It is also well known that
complications of tourniquet release has also been
associated with prolonged tourniquet inflation time.[2,3]
In our patient the cause of cardiac arrest can be
attributed to metabolic derangements. Application
and release of the extremity tourniquet causes several
metabolic changes.[1,4] Arterial pH, PaO2, PaCO2, lactic
acid and potassium levels change significantly after
release, the degree largely dictated by the duration
of ischemia time. Leakage of potassium, the major
intracellular cation leads to hyperkalemia in the early
reperfusion period, and has been implicated in sudden
mortality.[1]
To prevent complications one should be aware
of principles, pathophysiological changes and
complications associated with tourniquet use. With
advancement of technology, the risk of tourniquet
related complications have decreased. The use of
new tourniquet systems which prevent excessive
pressure build up[5] and the concept of Limb Occlusion
Pressure is important in safe and effective tourniquet
use. The other simple method is to add 50-75 mmHg
and 100-150 mm Hg above the limb systolic blood
pressure, for surgery on the upper limb and lower limb
respectively.[6] As anesthesiologists it is our primary
duty to create awareness among surgeons to follow the
standard accepted guidelines while using tourniquet
for surgeries.
BN Archana, P Vishnu Prasad, A Sreenivasa Babu
Department of Anesthesiology and Critical care, The Bangalore
Hospital, Bengaluru, Karnataka, India
237
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Letters to Editor
Address for correspondence:
Dr. BN Archana,
No.154, 2ndMain Road, Health Layout,
Annapooraneshwari Nagar, Nagharbhavi - 560 091,
Bengaluru, Karnataka, India.
Email drarchanabn@yahoo.co.uk
REFERENCES
1. MurphyCG, WinterDC, BouchierHayesDJ. Tourniquet
injuries: Pathogenesis and modalities for attenuation. Acta
Orthop Belg 2005;71:63545.
2. SapegaAA, HeppenstallRB, ChanceB, ParkYS, SokolowD.
Optimizing tourniquet application and release times in
extremity surgery. JBone Joint Surg Am 1985;67:30314.
3. HorlockerTT, HeblJR, GaliB, JankowskiCJ, BurkleCM,
BerryDJ, etal. Anesthetic, patient, and surgical risk factors for
neurologic complications after prolonged total tourniquet time
during total knee arthroplasty. Anesth Analg 2006;102:9505.
4. GirardisM, MilesiS, DonatoS, RaffaeliM, SpasianoA,
AntonuttoG. The hemodynamic and metabolic effects of
tourniquet application during knee surgery. Anesth Analg
2000;91:72731.
5. WakaiA, WinterDC, StreetJT, RedmondPH. Pneumatic
tourniquets in extremity surgery. JAm Acad Orthop Surg
2001;9:34551.
6. HorlockerTT, WedelDJ. Anaesthesia for Orthopaedic surgery.
In: BarashPG, CullenBF, StoeltingRK, CahalanMK, StockMC,
editors. Clinical Anesthesia. 6thed. Philadelphia: Lippincott
Williams and Wilkins; 2009. p.1338.
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DOI:
10.4103/0019-5049.130868
Anaesthetic management in a
patient with LennoxGastaut
syndrome
Sir,
LennoxGastaut syndrome(LGS), is an age specific
childhood epileptic encephalopathy characterised
by triad of multiple and frequent epileptic seizures
resistant to antiepileptic drugs, a characteristic
electroencephalogram(EEG), psychomotor delay and
behaviour disorder.[1] It occurs between 2 and 8years
of age. Diagnosis requires assessment of both clinical
and EEG features, to distinguish LGS from other
childhood epilepsy syndromes. Drop attacks are
common resulting in recurrent injury. About 60% of
children progress to status epilepticus. Management
options include antiepileptic drugs, ketogenic
238
diet, surgery(corpus callostomy) and vagus nerve
stimulation.
A 7yearold(21kg) patient was brought to the
emergency room with fracture of distal radius and
ulna. Afixation was planned. The parents gave a
history of LGS, indicating that she had multiple
seizures in a day. The fracture was due to a fall during
a drop attack. Her current antiepileptic medications
included valproic acid and lamotrigine 3times a day.
The morning dose of the drugs had been already
administered to the patient. Previous investigations
showed an unremarkable magnetic resonance
imaging brain, biotinidase deficiency, and a positive
2,4dinitrophenylhydrazine test. All other metabolic
tests and routine lab investigations were normal. The
EEG showed a frequent paroxysmal spike and wave
discharges of<2.5Hz.
An intravenous(IV) access was secured with the
patient in her mothers lap. Premedication of 1mcg/kg
of fentanyl and 0.5mg of midazolam helped separation
from her mother. Routine monitors were setup and the
patient induced with 5mg/kg of thiopentone sodium.
The anaesthesia was maintained throughout the
90min of the surgery with sevoflurane, oxygen and
nitrous oxide mixture on spontaneous ventilation
through a laryngeal mask airway with a JacksonRees
circuit. Incremental dose of 0.5mcg/kg of fentanyl
were administered 60min into the surgery. After the
surgery, the paediatric consultant requested that the
patient be taken for her routinely scheduled EEG.
Since the patient had regained consciousness in
the postanaesthesia care unit a bolus of 0.5mcg/kg
of dexmedetomidine was given to calm her down.
The patient was then transported to the EEG room
with the supporting monitoring equipment on an
adequately padded transport trolley. On reaching
the EEG room a continuous infusion of 0.3mcg/kg/h
of dexmedetomidine was established. The EEG was
recorded uneventfully. The patient was observed in
the post EEG recovery room until awake and then
released to her parents. During the entire process, she
had no obvious convulsion and postoperative period
was uneventful.
Concerns for the anaesthesiologists in such cases
include:(i) ability of the anaesthetics to modulate
or potentiate seizure activity;(ii) interactions
of anaesthetic drugs with antiepileptic agents;
(iii) perioperative care of epileptic patients;
(iv) associated comorbid conditions. (v) difficult
Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014