spinal anesthesia complications

1. Post spinal anesthesia
complications

2. Outline
• Management of hypotension after spinal block
• Management of PDPH
• Management of shivering after spinal
• Management of high /complete spinal
• Management of nausea & vomiting after spinal

3. Post spinal Hypotension:
Hypotension during induction of regional anaesthesia in
obstetric patients is associated with both maternal and fetal
morbidity.
The sympathectomy that occurs with neuraxial blockade
causes hypotension in women who receive spinal anaesthesia
for caesarean section.
Spinal hypotension can occur abruptly and may lead to
cardiovascular collapse. It causes maternal nausea and
vomiting and fetal acidosis

4. Hypotension caused by a reduction in SVR is normally
compensated by an increase in CO.
Under SA the increase in venous capacitance decrease CO,
because of veno -dilatation in the lower part of the body.
The situation is worsened in pregnancy by aortocaval
compression. Thus, more than 25%, CO usually decreases.
This is the combined effect of reduced cardiac output and
decreased SVR accounts for hypotension after spinal
anaesthesia.

5. The incidence => 80% ; the severity depends on the height
of the block, the position of the parturient, and whether
prophylactic measures were taken to prevent the hypotension.
Measures that decrease the risk of hypotension to varying
degrees include IV fluids, prevention of aorto-caval
compression, and monitoring of BP at frequent intervals after
placement of regional anesthetic.

6. General management
Large (16G) IV cannula (ensure adequate flow) prior to
neuraxial blockade
Establish baseline blood pressure
1 minute NIBP cycling post neuraxial blockade (until baby
delivered)
Apply wedge for left lateral tilt, consider full left lateral/asking
surgeon to lift the uterus if refractory hypotension

7. Management con…
Maintain SPB above 100 mmHg or >80% of pre-regional
blood pressure.
Bradycardia (HR<60 should be treated with atropine, if
accompanied with hypotension.
Do not use ephedrine before the baby is born.
Monitor blood loss to ensure that absolute hypovolemia does
not contribute to hypotension
Do not treat hypovolemia (eg hemorrhage) with vasopressors

8. Intravenous administration:
Crystalloid pre-loading has been shown to be clinically
ineffective at preventing hypotension.
Rapid crystalloid administration after induction of spinal
anaesthesia (coloading) provides better maternal blood
pressure control than pre-loading (Dyer et al. 2004)
but should be combined with the use of vasopressors to
prevent hypotension.

9. Crystalloid vs colloid
A recent systematic review found that crystalloid was
inconsistent in preventing hypotension and that colloid was
significantly better.
Dahlgren et al studied crystalloid compared with colloid for
preloading. Hypotension was significantly reduced after larger
volumes of colloid.

10. In another study of preloading comparing pentastarch with
crystalloid, French et al demonstrated a reduction in the
incidence of hypotension in the colloid group (12.5% versus
47.5%).
In contrast to these studies which all found colloid preload of
benefit, Karinen et al failed to find any reduction in the
incidence of hypotension when colloid was used

11. • Several recent studies have compared prehydration versus
cohydration both with crystalloids and colloids and shown that
haemodynamic changes and vasopressor requirement are
similar.
• Meta analysis (eight studies, 518 parturients),they found that
the incidence of hypotension to be similar for cohydration to
that of prehydration.

12. VASOPRESSORS
Ephedrine has been the drug of choice for more than 30 years in the
treatment of maternal hypotension in obstetric spinal anesthesia when
conservative measures fail.
Sympthomimetic with mixed effect.
Ephedrine has a slow onset of action making it difficult to
titrate and use it with an appropriate bolus dose.
As proved by various studies, a single prophylactic dose is
ineffective and the effectiveness depends on variable doses and
the rate of administration

13. Ephedrine depresses fetal PH more than Phenylephrine
– Ngan Knee et al demonstrated that ephedrine crosses placenta
more readily than phenylephrine.
Phenylephrine is a short-acting, potent, vasoconstrictor
that causes an increase in both systolic and diastolic blood
pressure.
– It counteracts the vasodilatation due to neuraxial anaesthesia
directly, restoring baseline blood pressure.
Traditionally, it was used as a second line vasoconstrictor
in obstetrics because of the concerns that it caused
vasoconstriction in the uteroplacental circulation.

14. When compared to ephedrine it has been shown to be:
- Easier to titrate
- Faster onset
- More effective at increasing systemic vascular resistance
- Causes less maternal tachycardia and hypertension
- Associated with improved fetal pH (Ngan Kee et al. 2003)

15. Phenylephrine can be administered by bolus or infusion.
A prophylactic bolus has been shown to be superior to a
therapeutic bolus with regards to incidence of hypotension,
NV(Das Neves et al. 2010).
Metaraminol:- a mixed alpha and beta agonist can be used for
spinal induced hypotension.
– Ngan Kee and colleagues demonstrated that Metaraminol was superior
to ephedrine at maintaining both maternal blood pressure and fetal pH
during spinal anesthesia for caesarean section.

16. PDPH
• Post-partum headache is the complaint of headache and neck
or shoulder pain in the first 6 weeks after delivery.
• Up to 39% of parturients experience headache in the first
postpartum week.
• Not all postpartum headache is PDPH, and as anaesthetists are
asked to review patients often, it is important to be aware of
the differential diagnoses

17. PDPH
• In parturients, the collective risk of unintentional dural
puncture with an epidural needle is ~1.5%, and of these,
52.1% will experience PDPH.
• After spinal injection, the incidence of headache ranges from
1.5 to 11.2%, depending on the size and type of needle.

18. PATHOGENESIS
CSF leakage into the epidural space via a tear in the dura.
CSF loss leads to a reduction in intracranial pressure and
downward traction on pain-sensitive intracranial
structures(veins, meninges and cranial nerves) resulting in a
headache that is classically worse in the upright position.
The fall in intracranial pressure may also cause
compensatory cerebro-vascular venodilation and this may
contribute to the development of the headache.

19. DIAGNOSIS AND DIFFERENTIAL
DIAGNOSIS
The fundamental principle in the assessment of any parturient with a
post-partum headache is to carefully consider the differential
diagnosis.
Infective: Meningitis, Encephalitis
Pharmacological/Metabolic:
Dehydration and Caffeine withdrawal
Vascular: Migraine, Cerebral vein thrombosis, Cerebral
infarction, Subdural haematoma & Subarachnoid haematoma

20. A history and examination should be performed taking account
of the timing of the headache in relation to the neuraxial
procedure, the nature of the headache as well as other
symptoms and signs.
In the case of a headache following a spinal procedure, PDPH
is more likely following dural puncture with a larger gauge
‘cutting’ tipped needle or after multiple attempts,
increasing the chance of a CSF leak.

21. Classic features of the headache caused by dural puncture:
Headache is often frontal-occipital.
Most headaches do not develop immediately after dural
puncture but 24-48 hours after the procedure with 90% of
headaches presenting within 3 days.
The headache is worse in the upright position and eases when
supine.
Pressure over the abdomen with the woman in the upright
position may give transient relief to the headache by raising
intracranial pressure secondary to a rise in intra-abdominal
pressure(Gutsche’s test).

22. Associated symptoms: neck stiffness, photophobia, tinnitus,
visual disturbance and cranial nerve palsies.
MRI may demonstrate diffuse dural enhancement and brain
descent.

23. MANAGEMENT
Conservative Management: Most post-dural puncture
headache will resolve spontaneously.
Conservative management has traditionally involved bed rest
and fluids though there is little evidence to support either of
these measures.
A recent Cochrane review concluded that routine bed rest after
dural puncture is not beneficial and should be abandoned.
While routine administration of additional fluids may be
unnecessary, avoidance of dehydration is advisable to help
limit headache severity. => traditional, lack evidence

24. Pharmacological
Many drugs have been recommended to treat PDPH, however
in the vast majority of cases, evidence of effectiveness is
limited.
Simple analgesia should be instituted in all patients with
PDPH; regular paracetamol and non-steroidal anti-
inflammatory medications may control symptoms adequately.

25. Caffeine:
Caffeine was first reported as a treatment for PDPH in 1949.
Caffeine is a central nervous system stimulant and is thought
to influence PDPH by inducing cerebral vasoconstriction.
Doses from 75 – 500 mg have been investigated and caffeine
has been administered orally, intramuscularly and
intravenously.
Caffeine is associated with adverse events including cardiac
arrhythmias and maternal seizures. In high doses (probably
>300mg) caffeine may enter breast milk and potentially lead to
neonatal irritability.

26. Many randomized trials failed to show superiority of caffeine
over other conservative methods to treat PDPH.
More recently, a randomized, double-blinded, placebo
controlled trial by Ragab and Facharzt in 2014 comparing
intravenous caffeine with placebo shows that IV caffeine can
be effective in reducing the rate and severity of PDPH.
– It may be that intravenous caffeine is effective while oral
caffeine is not.

27. Other conservative therapies being studied that have
also showed promising results.
A prospective, randomized, double-blinded, placebo-
controlled trial in which epidural morphine was
administered as 2- 3 mg dose 24 hours apart reduced
the incidence of PDPH from 48% to 12%

28. Invasive Management
• Epidural blood patch (EBP) after observation that patients
blood spinal tap at lumbar puncture were less likely to develop
PDPH.
• the first epidural blood patch was performed in 1960 by the
American surgeon, Dr James Gormley.
• Just 2 ml of the patient’s blood was injected during the first
epidural blood patch and the headache was relieved.

29. Epidural blood patching involves injection of autologous blood
into the epidural space.
It remains one of the few proven treatments of PDPH however
the mechanism of action remains unclear.
The resulting blood clot may have a “patch effect” on the dural
tear while the volume of blood transfused into the epidural
space raises intracranial pressure and reduces ongoing CSF
leak.

30. Effectiveness:
Early studies of the efficacy of EBP (up to 90%)
Permanent cure by a single blood patch can be expected
in 50% of patients.
About 40% of patients require a second blood patch
Despite the falling success rates, EBP remains the most
effective treatment for PDPH and has been shown in a
randomized controlled trial to be more effective than
conservative treatment in treating established PDPH.

31. Optimal Technique
EBP should be performed by two personnel, one an
experienced anaesthetist, the other competent in taking a
volume of blood from the arm. Both should employ full
aseptic precautions.
Contraindications to EBP include:
- Sepsis,
- Coagulopathy and
- Patient refusal.

32. EBP is likely to be most effective if performed at least 24
hours after the onset of PDPH.
Volumes of between 20-60mls of blood have been used.
Optimal volume is unknown but current recommendations
suggest 10 to 20ml should be injected

33. If the patient reports discomfort in the back during the
procedure the injection should be stopped.
The patient should lie flat for 1-2 hours after the procedure.
There is no evidence that bed rest for longer than this time is
beneficial.
Once discharged from hospital, follow up by telephone over
the first few days after EBP and review at 6 weeks is
recommended

34. Shivering:
Post-anesthetic shivering is spontaneous, involuntary ,
rhythmic , oscillating, tremor-like muscle hyperactivity that
increases metabolic heat production after general or regional
anesthesia.
The probable mechanisms could be decrease in core body
temperature secondary to:
– sympathetic block;
– peripheral vasodilatation;
– Increased cutaneous blood flow, which leads to increased heat loss
through skin;
– cold temperature of operation theatre; rapid infusion of cold IV fluids;
and effect of cold anaesthetic drugs upon the thermo sensitive receptors
in the spinal cord

35. Management:
Two approaches in the management of PAS:
1) Non-pharmacological methods and
2) Pharmacological methods

36. Non-pharmacological methods:
A number of physico-chemical methods helpful to prevent
PAS
There are three basic strategies for the prevention and
treatment of hypothermia and shivering:
(i) minimising redistribution of heat;
(ii) cutaneous warming during anaesthesia: Passive insulation/Active
warming
(iii) internal warming.
Minimising redistribution of heat
 This can be achieved by preoperative warming of peripheral tissues
 It minimise phase I hypothermia
 this would require subjecting patients to over 1 h of exposure to a
source of radiated heat pre-operatively

37.  Cutaneous warming during anaesthesia
1. Passive insulation
2. Active warming
 Internal warming

38. Review of literatures
9 RCTs for pethedine
4 RCT for tramadol, doxapram, and clonidine;
2 RCTs for nalbuphin
Evidence for these 5 drugs was found to be sufficient and
statistically significant.

39. Pethidine for treatment of PAS
Research has provided abundant documentation regarding
pethidine’s potent anti-shivering effects
However, the mechanism for these effects is poorly understood
This drug exerts its action on ĸ-opioid receptors (KOR) and μ-
opioid receptors (MOR),
– Researchers developed the theory that meperidine’s action on KOR
mediates its effect on PAS.

40. Tramadol
 A synthetic and centrally acting opioid
MOA:
• activating MORs and blocking norepinephrine and
serotonin reuptake
– 5 HT caused shivering and vasoconstriction
– Norepinephrine lowered the normal resting
temperature and attenuated the 5 HT induced
hyperthermia.
– The balance b/n 5 HT & norepinephrine inputs may
be responsible for thermoregulatory response.

41. Tramadol versus Pethidine
 All studies, whether RCTs or systematic reviews, found
tramadol as effective as meperidine
 However, researchers considered tramadol qualitatively
superior than pethidine due to:
• a faster onset
• Easily available
• no recurrence of shivering,
• shorter duration of recovery, and fewer adverse effects
• Three RCTs reported that tramadol 0.5 to 1 mg/kg was
effective

42. Clonidine
An alpha 2 adrenergic receptors agonist
It is effective at 0.15mg dose to treat PAS
 MOA
 The hypothalamus, where alpha 2 receptors are found, is
responsible for controlling body temperature.
 thought to work on hypothalamic receptors to inhibit
vasoconstriction and shivering or
 at other CNS levels by altering incoming thermal
information

43. Magnesium sulphate and ketamine
• competitive antagonist at NMDA-receptors and was found to
stop post-anaesthetic shivering

44. Management of accidental high spinal blockade
Complete spinal block is caused by local anaesthetic
interfering with the normal neuronal function in the cervical
spinal cord and brain stem.
RISK FACTORS:
 Drug factors
–dose
-Baricity
-Prior drug administration
Patient factors –
-body morphology
-Anatomical or pathological factors

45. Technique factors
1. Higher lumbar insertion may increase final block height
2. Position at and following injection – sitting may minimize
cephalad spread
3. Spinal needle – finer gauge and cephalad direction of needle
hole may increase risk of higher block

46. MANAGEMENT
Management is supportive and dependent on degree
and height of block.
Early recognition is vital as block progression may
be mitigated (reverse trendelenberg/head raised) or
serious cardio-respiratory compromise avoided.

47. Management:
FEATURE MANAGEMENT
Bradycardia Vagolytics eg. atropine
Hypotension Sympathomimetics eg.
ephedrine, adrenaline
Vasopressors eg. metaraminol,
phenylephrine Fluid boluses
Leg elevation
Respiratory dysfunction Oxygenation Intubation and
ventilation
Loss of consciousness Secure airway , supportive
measures

48. Nausea and vomiting

49. Mechanisms of Postoperative Nausea and Vomiting in
Regional Anesthesia
Several different mechanisms may play a role in causing
PONV in patients who receive regional anesthesia.
In a retrospective analysis, Crocker and Vandam found that
hypotension (systolic blood pressure <80 mmHg), a block
higher than T5.

50. Management:
• Phenothiazines:
Promethazine, prochlorperazine, and chlorpromazine are all
phenothiazines, exert their antiemetic effects by directly acting
on the central dopaminergic receptors of the chemoreceptor
trigger zone .
These agents are most effective in the treatment of opioid
induced PONV, but their use as the primary treatment for
PONV is limited by their tendency to cause sedation.

51. Butyrophenone
Droperidol is the only butyrophenone currently used in the
treatment of PONV.
Like the phenothiazines, droperidol acts competitively on
central dopaminergic receptors and is associated with sedation,
lethargy, agitation and extraphyramidal effects,

52. Antihistamines
Diphenhydramine, hydroxyzine, Vistaril®, and cyclizine
are all antihistamines which work to prevent nausea and
vomiting by acting on the H1 receptors.
Using as postoperative agents is limited by the excessive
sedation associated with administration.

53. Anticholinergic
Scopolamine is an anticholinergic agent that acts on the
muscarinic and histaminic receptors of the vestibular apparatus
used to reduce the incidence of PONV.
Very effective in patients treated with opioids ,
Complications: use is limited by a high incidence of sedation,
dry-mouth, dysphoria, confusion, disorientation, visual
disturbances and hallucinations.

54. Benzamides
Metoclopramide and trimethobenzamide are benzamides
– act on both central dopamine and serotonin receptors, with
both prokinetic and antiemetic effects.
Metoclopramide increases gastrointestinal tract motility,
decreasing gastric emptying time and gastric volume, and is
usually well tolerated in adult patients.

55. Serotonin antagonists
Ondansetron, granisetron, dolasetron, tropisetron and other
serotonin antagonists have been shown to provide effective
treatment and prophylaxis of PONV and are associated with a
low incidence of mild side effects.
– They are not dopamine, muscarinic or histamine receptor antagonists.
Others
Anxiolytics-Midazolam
Steroids=> Dexamethasone

56. THANK YOU!!!