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perfusion and no vascular sequelae. His limb mobility before induction and extreme care during regional
was preserved with good function. anaesthesia is important, especially avoiding epidural
anaesthesia.
EhlersDanlos syndrome is a disorder of connective
tissue and can be classified into at least ten types Kartik Syal, Dheeraj Singha, Ajay Sood
on the basis of clinical, genetic and biochemical Department of Anaesthesia, Indira Gandhi Medical College, Shimla,
Himachal Pradesh, India
information.[1] The fragile skin and loose joints is often
a result of abnormal genes that produce abnormal Address for correspondence:
proteins which confer an inherited frailty of collagen. Dr.Kartik Syal,
Among the different forms of EhlersDanlos syndrome, Department of Anaesthesia, Indira Gandhi Medical College,
Shimla, Himachal Pradesh, India.
typeIV has a high incidence of vascular damage and Email:kartik.syal@gmail.com
is also known as vascular EhlersDanlos syndrome,
possibly present in the present case, though without REFERENCES
the history of excessive bleeding or bruising.
1. Nerlich AG, Stss H, Lehmann H, Krieg T,
Mller PK. Pathomorphological and biochemical alterations
Patients with EhlersDanlos syndrome typeIV have in EhlersDanlossyndrome type IV. Pathol Res Pract
been classically described to have four distinctive 1994;190:697706.
2. GermainDP, HerreraGuzmanY. Vascular EhlersDanlos
features:[1] characteristic faces(long thin nose and lips, syndrome. Ann Genet 2004;47:19.
sunken cheeks and bulging or protruding eyes), very 3. GermainDP. Clinical and genetic features of vascular
thin and translucent skin, vascular fragility(tendency EhlersDanlos syndrome. Ann Vasc Surg 2002;16:3917.
4. PepinM, SchwarzeU, SupertiFurgaA, ByersPH. Clinical
to bruise easily and rupture of vessels, especially and genetic features of EhlersDanlos syndrome typeIV, the
the middle sized arteries) and rupture of viscera vascular type. NEngl J Med 2000;342:67380.
5. FallatM, HershJ, HJ. Theories on the relationship between
such as intestine and uterus.[2,3] Spontaneous
cryptorchidism and arthrogryposos. Pediatr Surg Int
rupture of arteries is the most common presenting 1992;7:2713.
symptom.[2] Most patients develop these complications 6. LiangMY, HankoE, DhameeMS. EhlersDanlos syndrome
typeIV: Anesthetic considerationsCase report. Middle East J
before the age of 40. Median age in these patients is Anesthesiol 2006;18:11859.
48years.[4] Cryptorchidism is frequently associated
with connective tissue disorder as the guiding Access this article online
descending track is defective.[5] Quick response code
Website:
www.ijaweb.org
Venous fragility can cause excessive blood loss, hence
adequate venous access, preferably elective central
line should be ensured before induction. If regional DOI:
10.4103/0019-5049.130846
anaesthesia is chosen, spinal anaesthesia has to be
performed carefully to reduce chances of vascular
trauma and it is possible that epidural anaesthesia
also can lead to significant bleed in these cases.
During general anaesthesia, there should be gentle Lifethreatening complication
laryngoscopy and intubation. Laxity of ligaments may
increase chances of atlantoaxial dislocations during
following infiltration with
forceful laryngoscopy. Laryngeal mask airway can adrenaline
cause increased pressures in pharyngeal areas, which
can lead to softtissue damage and vascular ooze.[6] The Sir,
positioning of patients is important with emphasis on
adequate padding of joints as skin trauma and also An 8yearold girl child of ASA PS Grade 1, weighing 22
nerve palsies can occur. kg, was posted for modified radical mastoidectomy for
chronic otitis media. In the operating room, necessary
Careful and precise surgical technique with monitoring and intravenous (IV) infusion of Ringer
meticulous haemostasis and availability of a vascular lactate was started. The induction was performed by an
surgeon is mandatory in these cases. High risk IV injection of propofol 40 mg, vecuronium 2 mg and
consent for vascular complications and subsequent fentanyl 30 g, and endotracheal intubation was carried
critical care should be taken. Good venous access out after adequate muscle relaxation. Anaesthesia was

Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014 225

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maintained with nitrous oxide(66 vol%) and isoflurane
(1 vol%) in O2. The depth of anaesthesia was adequate
as the vital parameters were stable and the patient was
receiving approximately a total MAC of 1.4 of inhalational
agents. After cleaning, painting and draping, the
surgeon injected 60g of adrenaline (3mL of 1:50,000
freshly prepared solution by diluting 1mg of adrenaline
in 49 mL of normal saline[NS]) subcutaneously at the
incision site behind the pinna after negative aspiration
over a period of 15-20 s. Within 30 s of the injection, the
heart rate(HR) and blood pressure(BP) increased from
106 beats per minute(bpm) to 200-210 bpm and from
110/70 to 198/110mmHg, respectively. The procedure
was stopped and the patient was administered 100%
O2. Within 2-3min, the airway pressures rose to 18
cmH2O from 10 cmH2O with coarse crepitations and
expiratory wheeze in all lung fields. There were no signs
of airway obstruction. O2 saturation (SpO2) was 85-90%
at FiO2 of 1. BP decreased to 75/40 mmHg with a HR
of 160-165 bpm. Lead II in the electrocardiogram(ECG)
showed sinus tachycardia. A provisional diagnosis of
acute congestive heart failure was made. Inj. furosemide
5 mg IV and Inj. dobutamine at 7g/kg/min were
administered. A urinary catheter was also inserted.
Intermittent IV doses of Inj. vecuronium 0.4 mg and
Inj. midazolam 0.4mg were given. Tracheal suctioning
revealed frothy secretions. Over a period of 1h, the
crepitations and wheeze gradually improved. BP could
be now maintained at 100/65mmHg without inotropes.
Urine output was 100mL. The SpO2 was 99% on FiO2
of 1. Arterial blood gas showed pH of 7.35, pCO2 of
45mmHg, pO2152 mmHg, BE3mmol/l and bicarbonate
of23mmmol/l. The trachea was extubated uneventfully
after administration of reversal agent.
After extubation, she was conscious and oriented. Her
vitals were satisfactory(HR 140 bpm, BP 100/55mmHg
without any inotropes, respiratory rate 25/min) SpO2
was92% on air and 96% on venturi mask with FiO2
of 0.4. Auscultation showed few crepitations at the base
of the lungs with normal heart sounds. The patient was
shifted to the intensive care unit. Chest Xray, 12lead
ECG, 2D ECHO and serum electrolytes were normal
and she was discharged from the ICU after 2days.
Skin and subcutaneous tissue infiltration with
adrenaline prior to incision is a common practice in
an attempt to decrease the vascularity of the tissues,
which improves the surgical field view and reduces
the blood loss while operating on a vascular field like
head and neck surgeries. The maximum recommended
dose of adrenaline for infiltration is 5-10g/kg, which
226
may get altered due to simultaneous administration of
inhaled anaesthetic agents.[1] It is noted that inhalational
agents slow the automaticity of the sinoatrial node and
myocardial conduction, resulting in atrial and ventricular
arrhythmias, which are further potentiated by the use
of exogenous adrenaline.[2,3] Johnston etal. calculated
the ED50 of adrenaline that produces arrhythmia with
halothane to be 2.1g/kg and with isoflurane to be
6.7 g/kg.[1] However, there are case reports suggesting
the occurrence of severe hypertension, tachycardia,
pulmonary oedema, lifethreatening arrhythmias
and cardiac arrest on infiltration of only 20-30g of
adrenaline.[4,5]
Adding lignocaine to epinephrine has a protective
actionagainst cardiovascular complications as it
stabilizes the myocardium by blocking sodium
channels.[1,6] It is found that for subcutaneous
infiltration, using 1:100,000 solution caused significant
tachycardia than the 1:200,000 solution, and the
1:500,000 solution is virtually free of any sideeffects
with a significant decrease in blood loss.[7,8]
In our case, the surgeon slowly injected 60g of
adrenaline for infiltration, which was well within
the recommended doses. The cardiovascular crisis
precipitated by the small dose was unexpected and
dramatic. It could be due to accidental intravascular
placement of the drug. Repeated aspirations while
injecting are recommended. Using 1-2% lignocaine
with adrenaline for infiltration is preferred as it has
a protective action against arrhythmias, but, in our
case, adrenaline was diluted in NS. Also, 1:50,000
adrenaline was used as compared with the standard
recommended concentration of 1:100,000-1:200,000.
Thus, it can be concluded that there are chances
of severe cardiovascular crisis even after small
recommended doses of adrenaline. Hence, one should
be cautious while adrenaline is being injected.
Neha Gupta, Veena Gupta
Department of Anaesthesia, Maharani Laxmi Bai Medical College,
Jhansi, Uttar Pradesh, India
Address for correspondence:
Dr. Neha Gupta,
H7, Veerangana Nagar, Kanpur Road,
Jhansi284128, Uttar Pradesh, India.
Email:neyz181@yahoo.co.in
REFERENCES
1. JohnstonRR, Eger EI II, WilsonCA comparative interaction of
epinephrine with enflurane, isoflurane, and halothane in man.
Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
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Letters to Editor
Anesth Analg 1976;55:70912.
2. Atlee JL 3rd, BosjnakZJ. Mechanisms for cardiac dysrhythmias
during anesthesia. Anesthesiology 1990;72:34774.
3. KatzRL, KatzGJ. Surgical infiltration of pressor drugs and their
interaction with volatile anaesthetics. Br J Anaesth 1966;38:7128.
4. WanamakerHH, ArandiaHY, WanamakerHH. Epinephrine
hypersensitivityinduced cardiovascular crisis in otologic
surgery. Otolaryngol Head Neck Surg 1994;111:8414.
5. WoldorfNM, PastorePN. Extreme epinephrine sensitivity with
a general anesthesia. Arch Otolaryngol 1972;96:2727.
6. MurthyHS, RaoGS. Cardiovascular responses to scalp
infiltration with different concentrations of epinephrine
with or without lidocaine during craniotomy. Anesth Analg
2001;92:15169.
7. HardwickeJT, JordanRW, SkillmanJM. Infiltration of
epinephrine in reduction mammoplasty: Asystematic review
of the literature. Plast Reconstr Surg 2012;130:7738.
8. ThomasSS, SrivastavaS, NancarrowJD, MohmandMH.Dilute
adrenaline infiltration and reduced blood loss in reduction
mammaplasty.Ann Plast Surg 1999;43:12731.
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DOI:
10.4103/0019-5049.130850
Sinus arrest with intrathecal
dexmedetomidine
Sir,
Dexmedetomidine, a highly selective 2 adrenoceptor
agonist, is being increasingly used as an adjuvant
in neuraxial blocks as it prolongs the sensory and
motor block in a dose-dependent manner.[1] Severe
bradycardia and cardiac arrest has been reported with
the intravenous use of dexmedetomidine.[2,3] However,
severe bradycardia progressing to sinus arrest after
intrathecal administration of dexmedetomidine has
not been reported.
A 40-year-old female, 155cm in height and weighing
65kg, was scheduled for total abdominal hysterectomy.
She had been operated for myomectomy under
spinal anaesthesia 5years back. Her general physical
examination and all routine investigations were
unremarkable. Upon arrival in the operating room,
monitors were attached and her vitals were recorded.
Aperipheral venous access was established and pre-
loaded with 500 mL of Ringer lactate. The subarachnoid
space was reached in the L2-L3 interspace using a 25G
Quinckes needle with the patient in the left lateral
Indian Journal of Anaesthesia | Vol. 58 | Issue 2 | Mar-Apr 2014
position. After ensuring free flow of cerebrospinal
fluid, 2.5 mL of hyperbaric bupivacaine with 10g of
dexmedetomidine was administered. The patient was
positioned supine and oxygen was administered via a
face mask at a rate of 5 L/min.
The level of sensory block to pinprick was T10 after
2min, and T6 was the highest level of sensory block
achieved. The surgery commenced and the patients
heart rate remained in the range of 50-60/min, with
the blood pressure at around 130/80 mmHg. After
about 70min, when the surgeons were suturing the
peritoneum, there was a sudden drop in her heart
rate to 40/min. Immediately, the surgical handling
was stopped and injection atropine 0.6 mg was given
intravenously, to which there was no response for
3min. Meanwhile, she complained of some discomfort
in her epigastrium and her heart rate further dropped
to 34/min while her blood pressure was 124/76 mmHg
with SpO2 of 99%. Another dose of inj. atropine 0.6mg
was given intravenously but her heart rate dropped to
18/min over 5 s followed by sinus arrest. Then, the
third dose of inj. atropine 0.6mg was given, which led
to an increase in her heart rate to 86/min. The level of
sensory blockade was T10 at this time and the SpO2 was
consistently 99%. The surgery was completed in the
next 15min uneventfully and the estimated blood loss
was around 200 mL. The patient remained comfortable
with a heart rate of around 74/min and blood pressure
of 124/86mmHg. Her post-operative Holter monitoring
and echocardiography were unremarkable.
Intrathecal dexmedetomidine when combined
with spinal bupivacaine produces earlier onset and
prolonged duration of sensory and motor block with
excellent quality of post-operative analgesia without
significant haemodynamic alterations.[1,4] Although
episodes of sinus arrest and severe bradycardia
progressing to asystole have been reported in patients
receiving intravenous dexmedetomidine,[2,3] no severe
cardiovascular complications have been observed
with intrathecal dexmedetomidine. Two cases of
bradycardia (heart rate 50/min) have been observed by
Gupta et al. when they used 5 g of dexmedetomidine as
an intrathecal adjuvant for post-operative analgesia.[5]
The two very unusual features observed in our case
were the time to the occurrence of sinus arrest and the
high dose of atropine required for its treatment. As 1
h had elapsed between the intrathecal administration
of drugs and the sinus arrest, sinus arrest due to
sympathetic blockade due to bupivacaine was less
227