By Dr SajidaPharm D 16th May

The first spinal analgesia was administered in 1885 by Leonard Corning (1855–1923), a neurologist in New York.[1] He was experimenting with cocaine on the spinal nerves of a dog when he accidentally pierced the dura mater.

The first planned spinal anaesthesia for surgery in man was administered by August Bier (1861–1949) on 16 August 1898, in Kiel, when he injected 3 ml of 0.5% cocaine solution into a 34-year-old labourer.[2] After using it on 6 patients, he and his assistant each injected cocaine into the other's spine. They recommended it for surgeries of legs, but gave it up due to the toxicity of cocaine.

Defination local anesthetic injection into lumbar subarachnoid space.Site of action:

◦ Primary: preganglionic fibers leading the spinal cord in the anterior rami

◦ Secondary: superficial spinal cord layers Mechanism Regardless of the anaesthetic agent (drug) used, the desired effect to block the transmission of afferent nerve signals from peripheral

nociceptors. Sensory signals from the site are blocked, thereby eliminating pain.

Most commonly used agents:Tetracaine (pontocaine), lidocaine (Xylocaine), bupivacaine (Marcaine)

Characteristics of some drugs: Bupivacaine (Marcaine):

More effective than tetracaine (pontocaine) in preventing lower-extremity tourniquet pain (orthopedic surgery cases)

Chloroprocaine (Nesacaine) Not placed in subarachnoid space due to neurotoxicity

risk

Specific gravity of the local anesthetic solution

 Glucose addition: increased specific gravity above that of CSF (hyperbaric)

 Distilled water addition: decreased specific gravity below that of CSF (hypobaric)

◦ Consequences of sympathetic blockade:  Arteriolar dilation  No significant effect on systemic BP due to compensatory

upper extremity vasoconstriction. No cerebrovascular vasoconstriction Total sympathetic blockade due to spinal anesthesia: associated with

a reduction in systemic vascular resistance of < 15%. Rationale: arteriolar smooth muscle does not dilate maximally

because of intrinsic tone  Many major cardiovascular response secondary to spinal

anesthesia due to:  Effects on venous circulation  Venules: minimal intrinsic tone retention; maximal dilation during

spinal anesthesia

 Cardiac slowing (bradycardia) secondary to blockade of preganglionic cardiac accelerator nerves (T1 to T4)

 This bradycardia response may be worsened in the presence of reduced preload and as a result, reduce stimulation of atrial stretch receptors (which, when activated, cause cardioacceleration)

 Management of bradycardia secondary to T1 to T4 blockade may include administration of low-dose epinephrine {Clark Albert, MD, personal communication}

Non-availability of patient's consent, local infection or sepsis at the site of lumbar puncture, bleeding disorders, space occupying lesions of the brain, disorders of the spine and maternal hypotension.

All surgical interventions below the umbilicus, is the general guiding principle:

Abdominal & vaginal hysterectomies Laparoscopy Assisted Vaginal Hysterectomies (LAVH

) combined with general anaesthesia

Caesarean sections Hernia (inguinal or epigastric) Piles fistulae & fissures orthopaedic surgeries on the pelvis, femur, tibia and

the ankle nephrectomy cholecystectomies trauma surgery on the lower limbs, especially if the

patient is full-stomach Open tubectomies Transurethral resection of the prostate

Spinal anaesthetics are typically limited to procedures involving most structures below the upper abdomen. To administer a spinal anaesthetic to higher levels may affect the ability to breathe by paralysing the intercostal respiratory muscles, or even the diaphragm in extreme cases (called a "high spinal", or a "total spinal", with which consciousness is lost), as well as the body's ability to control the heart rate via the cardiac accelerator fibres.

Also, injection of spinal anaesthesia higher than the level of L1 can cause damage to the spinal cord, and is therefore usually not done.

Primary Reference: Stoelting, R.K., "Local Anesthetics", in

Pharmacology and Physiology in Anesthetic Practice, Lippincott-Raven Publishers, 1999, pp 158-181.;Miller, R.D., Local Anesthesia, in

Basic and Clinical Pharmacology, (Katzung, B. G., ed) Appleton-Lange, 1998, pp 425-433.