Effect of neuraxial block on renal and GIT functions Rasha Mahmoud

Introduction: Neuraxial anesthesia is the name used for spinal, epidural and caudal blocks. Each of these different blocks can be achieved either with a single injection or through intermittent boluses or constant infusions delivered through a catheter.  

Indications for neuraxial blockade include: 1) Surgery of lower abdominal, inguinal, urogenital, gynecologic and rectal regions and the lower extremity including orthopedic and vascular procedures 2) Obstetrics •Labor analgesia •Surgical anesthesia for c-sections 3) Post-operative pain control •Thoracic surgery •Major abdominal surgery •Orthopedic surgery (hip, knee) 4) Pain Control •Rib fractures

Contraindications: Absolute: patient refusal-bleeding diathesis-infection at the proposed site of injection-severe hypovolemia-elevated intracranial pressure. Relative: Sepsis – uncooperative patient - severe spinal deformity- demyelinating lesion - severe stenotic heart valvular disease or ventricular outflow obstruction. Controversial: Prior back surgery at injection site- prolonged and complicated operation with severe blood loss.  

Sites of Action: The main site of action for neuraxial blockade is the nerve root. In spinal blocks, LA is injected around the nerve root in the subarachnoid space. Direct injection into the CSF allows a relatively small dose and volume to achieve a dense sensory and motor blockade. In epidural and caudal blocks, LA is injected into the epidural space to bathe the nerve root. In contrast to spinal blocks, a higher volume and dose of LA is needed to achieve the same concentration of LA.

Mechanism of Action: Conduction blockade of posterior nerve roots interrupts somatic and visceral sensation whereas blockade of anterior nerve root fibers prevents efferent motor and autonomic transmission.

Somatic and Motor Blockade: Blocking painful stimuli and abolishing skeletal muscle tone is ideal for surgical procedures, providing analgesia and muscle relaxation.  Smaller and myelinated fibers are blocked before larger, unmyelinated fibers. This and the fact that the concentration of LA decreases with increasing distance from the site of injection leads to the phenomenon of differential blockade.

Differential blockade: sympathetic blockade (tested by temperature) occurs two levels above….. sensory blockade (tested by pin prick or light touch) occurring two levels above…. motor blockade  

Autonomic Blockade: Interruption of efferent autonomic transmission at spinal nerve roots produces sympathetic and some parasympathetic blockade. Sympathetic nerve fibers exit from T1-L2 (thoracolumbar) while parasympathetic exit with cranial and sacral nerves (craniosacral). Neuraxial anesthesia doesn’t block the vagus nerve. What results from blockade is either decreased sympathetic tone or unopposed parasympathetic tone.

The three most important factors in determining the level of the spinal blockade are: Baricity of the local anesthetic solution Position of the patient during and after injection Dose of the anesthetic injected

Complications of spinal blockade include: local anesthetic neurotoxicity neurologic injury PDPH high spinal blockade and cardiovascular collapse.

Physiologic Effects of Neuraxial Blockade : Normal physiologic manifestations of neuraxial blockade such as hypotension are not necessarily complications but normal physiological effects of neuraxial blockade. These effects involve various system: cardiovascular , respiratory, gastrointestinal, renal and endocrine. In this section we will briefly discuss impacts of neuroaxial blockade on the renal and GIT functions

Effects on renal function: Renal function is intimately related to renal blood flow. Blood flow to both kidneys is 20-25% of cardiac output.

The effect of neuraxail block on the renal blood flow is closely related to the cardiovascular system effects of the block, particularly: hypotension. Neuraxial blockade can impact the cardiovascular system by causing the following changes: 1. Decrease in blood pressure (33% incidence of hypotension in non-obstetric populations) 2. Decrease in heart rate (13% incidence of bradycardia in non-obstetric populations) 3. Decrease in cardiac contractility

Sympathectomy is directly related to the height of the block and results in venous and arterial vasodilatation. Total peripheral vascular resistance in the normal patient (normal cardiac output and normovolemic) will decrease 15-18%. In the elderly the systemic vascular resistance may decrease as much as 25% with a 10% decrease in cardiac output. Heart rate may decrease during a high block due to blockade of the cardio accelerator fibers (T1-T4).

Neuraxial blockade has little effect on the blood flow to the renal system. Auto regulation maintains adequate blood flow to the kidneys as long as perfusion pressure is maintained. The kidneys remain per fused when the MAP remains above 50mmHg. Transient decreases in renal blood flow may occur when MAP is less than 50 mm Hg, but even after long decreases in MAP, renal function returns to normal when blood pressure returns to normal.

One aspect of genitourinary function that is of clinical importance is the belief that neuraxial blocks are a frequent cause of urinary retention, which either delays discharge of outpatients or necessitates bladder catheterization in inpatients. It is clear that lower concentrations of local anesthetic are necessary for paralysis of bladder function than for motor nerves to lower extremities.

Innervations of urinary bladder: Parasympathetic (S2-S4): pelvic plexus supplying bladder and sphincter Sympathetic (T10-L2):supplying bladder base , internal sphincter and proximal urethera Somatic (S2-S3): pudendal nerve supplying external sphincter Somatic afferent in pudendal nerve Visceral afferent in autonomic system

When activated, the primary role of the parasympathetic innervation to the bladder is detrusor contraction and bladder emptying. Sympathetic innervation to the bladder causes the bladder neck and proximal urethra to contract and the body to relax. The net effect of sympathetic stimulation is urine storage.

Voiding can be initiated or inhibited by higher center control of the external sphincter. Innervations of the lower urinary tract can be simplified as a micturation reflex with modification from higher cortex.

Neuraxial blockade effectively blocks sympathetic and parasympathetic control of the bladder at the lumbar and sacral levels. Urinary retention can occur due to the loss of autonomic bladder control. Detrusor function of the bladder is blocked by local anesthetics. Normal function does not return until sensory function returns to S3.

Risk factors for prolonged blockade of the detrusor muscle include the use of long acting local anesthetics, age > 50 years, volume of fluids administered, and surgical procedure. Urinary retention is More common with neuraxial opioid administration Interaction with opioid receptors in the sacral spinal cord Inhibition of sacral parasympathetic nervous system outflow Detrusor muscle relaxation Increased maximum bladder capacity Urinary retention  

Prolonged blockade of the detrusor muscle may lead to bladder over distention and urinary retention. This should be taken into consideration if no urinary catheter will be placed. If possible, short acting medications should be used. The anesthesia provider should monitor the amount of intravenous fluids administered. The patient with a history of an enlarged prostrate is at risk for urinary retention. Patients should be monitored for urinary retention.

Effects on the GIT functions The sympathetic innervation to the abdominal organs arises from T6 to L2. Due to sympathetic blockade and unopposed parasympathetic activity after spinal blockade, secretions increase, sphincters relax, and the bowel becomes constricted.

Nausea and vomiting occur after spinal anesthesia approximately 20% of the time. Risk factors include blocks higher than T5, hypotension, opioid administration, and a history of motion sickness. Increased vagal activity after sympathetic block causes increased peristalsis of the gastrointestinal tract, which leads to nausea. Accordingly, atropine is useful for treating nausea after high spinal blockade.

Postoperative epidural analgesia enhances the return of gastrointestinal function. When epidural analgesia is continued into the postoperative period, there may be a protective effect on the gastric mucosa because intramucosal pH is higher during postoperative epidural analgesia than with systemic analgesia.  

Effects on the liver functions Hepatic blood flow correlates to arterial blood flow. There is no auto regulation of hepatic blood flow. If the anesthesiologist maintains mean arterial pressure (MAP) after placing a spinal anesthetic, hepatic blood flow will be maintained. Patients with hepatic disease must be carefully monitored and their blood pressure must be controlled during anesthesia to maintain hepatic perfusion.

In patients with liver disease either regional or general anesthesia can be given, as long as the MAP is kept close to baseline. seen. Spinal and epidural anesthesia carries the risk of epidural hematoma and paralysis if there is abnormal clotting in liver diseases but there are otherwise no special precautions. The half-life of lignocaine is prolonged in liver failure but this is not significant when used in regional anesthesia.

Thank you

Brown, D. L. (2005). Spinal, epidural, and caudal anesthesia. In R. D Brown, D.L. (2005). Spinal, epidural, and caudal anesthesia. In R.D. Miller Miller’s Anesthesia, 6th edition. Philadelphia: Elsevier Churchill Livingstone. Klein man, W. & Mikhail, M. (2006). Spinal, epidural, & caudal blocks. In G.E. Morgan et al Clinical Anesthesiology, 4th edition. New York: Lange Medical Books. Reese, C.A. (2007). Clinical Techniques of Regional Anesthesia. Park Ridge, Il: AANA Publishing. Warren, D.T. & Liu, S.S. (2008). Neuraxial Anesthesia. In D.E. Longneck et al (eds) Anesthesiology. New York: McGraw-Hill Medical.

Control of renal blood flow: Intrinsic control (auto regulation) maintains renal blood flow normally in the range 80-180 mmHg mean blood pressure. This may be due to an intrinsic myogenic response of afferent arterioles. Outside the auto regulation limits , RBF (and glomerular filtration rate ) becomes pressure dependent. Glomerular filtration stops when mean blood pressure is less than 40-50 mmHg.

Extrinsic control: Includes vasoconstrictors and vasodilators Salt retaining systems protect against: hypovolemia hypotension and hyponatremia They include: sympatho-adrenal system- Renin-angiotensin-aldosterone system - Arginine vasopressin (ADH) – Endothelin and Serotonin Vasodilators they are the salt excreting systems, they protect against hypervolemia ,Hypertension and hypernatrremia Prostaglandins, Atrial natriuretic peptide, Nitric oxide and Dopamine

Effects on renal function: Kidney functions: Regulation of electrolytes, Maintenance of acid base balance, Regulation of blood pressure. Essential in the urinary system, Produce urine and excrete wastes. Reabsorption of water, glucose and amino acids. Produce hormones e.g. erythropoietin. Renal function is intimately related to renal blood flow. Blood flow to both kidneys is 20-25% of cardiac output.

Functions of the micturation system: Passive reservoir for temporary storage of urine. Active function for eliminating urine from the reservoir at an appropriate time.  

Gastrointestinal Effects: Functions of the GIT: Digestive: continual supply of water, electrolytes, and nutrients from the external medium to the internal medium Innate immunity: (results from general processes): destruction of swallowed organisms by the acid secretions of the stomach and by the digestive enzymes Endocrine: secretion of gastric, cholecystokinin (CCK), secretion, vasoactive intestinal peptide (VIP), gastric inhibitory peptide (GIP), etc

Effects of neuraxial block on the liver functions: Functions of the liver: Detoxification, protein synthesis, production of biochemical necessary for digestion, glycogen storage, decomposition of red blood cells and others. The liver's highly specialized tissues regulate a wide variety of high-volume biochemical reactions, including the synthesis and breakdown of small and complex molecules, many of which are necessary for normal vital functions. The liver is necessary for survival.