Spinal Anesthesia Side Effects

Spinal Anesthesia Side Effects

Spinal anesthesia is a quick and usually easy way of completely numbing a specific part of the body for surgery or other painful medical procedures. A trained anesthesiologist injects anesthesia into the lower back. Obstetricians frequently use spinal anesthesia to ease pain during childbirth and to keep the mother awake during a Cesarean section. Post spinal anesthesia side effects can vary, but are usually not too serious

Headaches

1. The No. 1 side effect of spinal anesthesia is headaches. Younger people seem more likely to get a headache after spinal anesthesia. The headache can usually be treated with pain medication or even caffeine. If the headache doesn't go away, the doctor may try an epidural blood patch, which usually gives relief immediately.

   Low Blood Pressure

2. Some patients may have low blood pressure after spinal anesthesia. This is usually the result of dehydration. Doctors usually insist the patient drink plenty of water after spinal anesthesia.

   Painful Bladder

3. Occasionally, a patient will have a painful bladder after spinal anesthesia. This is caused by urinary retention which distends the bladder, resulting in pain. If the patient can't urinate on his own, he may need to have his bladder catheterized.

   Neurological Damage

4. Neurological damage is very rare, although patients are frequently concerned about it. If an epidural vein is damaged during the procedure, a hematoma may occur. A hematoma is a collection of blood which is ripe for infection. Fortunately this hardly ever happens in patients who clot normally.

   Unusual Side Effects

5. Other rare side effects include nerve damage, backache, decrease in sexual function and allergic reactions.

Spinal anaesthesia: Choice of needle

Quincke
Short bevelled, cutting tip. Insertion results in the needle cutting parallel to the dura fibres.
Whitacre
Designed to spread the dural fibres and help reduce the occurrence of post-dural puncture headache. Yields a distinct "pop" as the pencil point penetrates the dura.
Sprotte
As the fibres of the dura run parallel to the long axis of the spine, if the bevel of the needle is parallel to them, it will part rather than cut them, and therefore leave a smaller hole.

The incidence of post-dural puncture headache (PDPH) after the use of a standard spinal needle (Quincke) is dependent on the size of the needle. In young female patients, the mean incidence of PDPH is approximately 15% when using a 25G needle and around 5% when using a 26G needle. A significant reduction in PDPH from 6.3% to 2.5% is seen if using a 27G needle instead of a 26G needle in obstetric patients. The incidence can be further reduced by puncturing the dura parallel to the dural fibres.

Newer spinal needles with special tip design (modifications of the original pencil point Whitacre needle) have lowered the incidence of PDPH to an acceptable level.

In 1987, Sprotte et al. introduced the 'atraumatic' spinal needle (a modified pencil point needle) and reported that the incidence of PDPH could be reduced to less than 1%. However, a higher failure rate was reported and related to the dimensions and placement of the sideport of this needle. The modern Whitacre needles, with a smaller sideport closer to the tip, are superior to the Sprotte® needle and their use has reduced the incidence of significant PDPH to less than 1%.

Vaporizers (تبخیر کننده)

Processing: Vaporizers

Physical principles

Vapor pressure Molecules escape from a volatile liquid to the vapor phase, creating a "saturated vapor pressure" at equilibrium. Vapor pressure (VP) increases with temperature. VP is independent of atmospheric pressure, it depends only on the physical characteristics of the liquid, and its temperature.

Latent heat of vaporization is the number of calories needed to convert 1 g of liquid to vapor, without temperature change in the remaining liquid. Thus, the temperature of the remaining liquid will drop as vaporization proceeds, lowering VP, unless this is prevented.

Specific heat is the number of calories needed to increase the temperature of 1 g of a substance by 1 degree C. Manufacturers select materials for vaporizer construction with high specific heats to minimize temperature changes associated with vaporization.

Thermal conductivity - a measure of how fast a substance transmits heat. High thermal conductivity is desirable in vaporizer construction.

Classification

Dräger Vapor 19.1, Vapor 2000, Penlon Sigma, Datex-Ohmeda S/5 ADU Aladin vaporizers, and Datex-Ohmeda Tec 4, 5 are classified as

Variable bypass

Fresh gas flow from the flowmeters enters the inlet of any vaporizer which is on. The concentration control dial setting splits this stream into bypass gas (which does not enter the vaporizing chamber), and carrier gas (also called chamber flow, which flows over the liquid agent).

Flow over

Carrier gas flows over the surface of the liquid volatile agent in the vaporizing chamber, as opposed to bubbling up through it (as in the copper kettle and Vernitrol)

Temperature compensated

Equipped with automatic devices that ensure steady vaporizer output over a wide range of ambient temperatures

Agent-specific

Only calibrated for a single gas, usually with keyed fillers that decrease the likelihood of filling the vaporizer with the wrong agent

Out of circuit

Out of the breathing circuit, as opposed to (much) older models such as the Ohio #8 (Boyle's bottle) which were inserted within the circle system.

The copper kettle and Vernitrol are measured-flow, bubble-through, non-temperature compensated, multiple agent, and out of circuit 

Vaporizer Models

Classification	Datex-Ohmeda Tec 4, Tec 5, SevoTec, and Aladin (AS/3 ADU); Dräger Vapor 19.n, Vapor 2000	Copper Kettle, Vernitrol	Datex-Ohmeda Tec 6 (Desflurane)
Splitting ratio (carrier gas flow)	Variable-bypass (vaporizer determines carrier gas split)	Measured-flow (operator determines carrier gas split)	Dual-circuit (carrier gas is not split)
Method of vaporization	Flow-over (including the Aladin for desflurane, which does not require added heat like the Tec 6)	Bubble-through	Gas/vapor blender (heat produces vapor, which is injected into fresh gas flow)
Temperature compensation	Automatic temperature compensation mechanism	Manual (i.e., by changes in carrier gas flow)	Electrically heated to a constant temperature (39ºC; thermostatically controlled)
Calibration	Calibrated, agent-specific	None; multiple-agent	Calibrated, agent-specific
Position	Out of circuit	Out of circuit	Out of circuit
Capacity	Tec 4: 125 mL Tec 5: 300 mL Vapor 19.n: 200 mL Aladin: 250 mL	200-600 mL (no longer manufactured)	390 mL

Epidural Anesthesia (بیحسی اپیدورال)

 

Epidural anesthesia is the most popular means for pain relief during labor. In fact, more women ask for an epidural by name than any other method of pain relief. Over 50% of women giving birth at hospitals use epidural anesthesia.

As you prepare yourself for “labor day”, learn as much as possible about pain relief options so you will be equipped and ready to make decisions throughout your birth experience. Understanding the different types of epidurals, how an epidural is administered, and the benefits and potential risks of an epidural will prepare you to make an informed decision for you and your baby as your birth unfolds.

     ?What is epidural anesthesia

Epidural anesthesia is regional anesthesia that blocks pain in a particular region of the body. The goal of an epidural is to provide analgesia, or pain relief, rather than complete anesthesia, which is total lack of feeling. Epidurals block the nerve impulses from the lower spinal segments resulting in decreased sensation in the lower half of the body. Epidural medications fall into a class of drugs called local anesthetics, such as bupivacaine, chloroprocaine, or lidocaine. They are often delivered in combination with opioids or narcotics, such as fentanyl and sufentanil, to decrease the required dose of local anesthetic. This way pain relief is achieved with minimal effects. These medications may be used in combination with epinephrine, fentanyl, morphine, or clonidine to prolong the epidural’s effect or stabilize the mother’s blood pressure

Epidural Hematoma

Epidural hematoma (EDH) is a traumatic accumulation of blood between the inner table of the skull and the stripped-off dural membrane. The inciting event often is a focused blow to the head, such as that produced by a hammer or baseball bat. In 85-95% of patients, this type of trauma results in an overlying fracture of the skull. Blood vessels in close proximity to the fracture are the sources of the hemorrhage in the formation of an EDH. Because the underlying brain has usually been minimally injured, prognosis is excellent if treated aggressively. Outcome from surgical decompression and repair is related directly to patient's preoperative neurologic condition.

Pathophysiology

Approximately 70-80% of EDHs are located in the temporoparietal region where skull fractures cross the path of the middle meningeal artery or its dural branches. Frontal and occipital EDHs each constitute about 10%, with the latter occasionally extending above and below the tentorium. Association of hematoma and skull fracture is less common in young children because of calvarial plasticity.

EDHs are usually arterial in origin but result from venous bleeding in one third of patients. Occasionally, torn venous sinuses cause EDH, particularly in the parietal-occipital region or posterior fossa. These injuries tend to be smaller and associated with a more benign course. Usually, venous EDHs only form with a depressed skull fracture, which strips the dura from the bone and, thus, creates a space for blood to accumulate. In certain patients, especially those with delayed presentations, venous EDHs are treated nonsurgically.

Expanding high-volume EDHs can produce a midline shift and subfalcine herniation of the brain. Compressed cerebral tissue can impinge on the third cranial nerve, resulting in ipsilateral pupillary dilation and contralateral hemiparesis or extensor motor response.

EDHs are usually stable, attaining maximum size within minutes of injury; however, Borovich demonstrated progression of EDH in 9% of patients during the first 24 hours¹. Rebleeding or continuous oozing presumably causes this progression. An EDH can occasionally run a more chronic course and is detected only days after injury.

Frequency

United States

EDH occurs in 1-2% of all head trauma cases and in about 10% of patients who present with traumatic coma.

Mortality/Morbidity

• Reported mortality rates range from 5-43%.
• Higher rates are associated with the following:
  • Advanced age
  • Intradural lesions
  • Temporal location
  • Increased hematoma volume
  • Rapid clinical progression
  • Pupillary abnormalities
  • Increased intracranial pressure (ICP)
  • Lower Glasgow coma scale (GCS)
• Mortality rates are essentially nil for patients not in coma preoperatively and approximately 10% for obtunded patients and 20% for patients in deep coma.

Age

• Patients younger than 5 years and older than 55 years have an increased mortality rate.
• Patients younger than 20 years account for 60% of EDHs.
• EDH is uncommon in elderly patients because the dura is strongly adhered to the inner table of the skull. In case series of EDH, fewer than 10% of patients are older than 50 years.

Clinical

History

• Fewer than 20% of patients demonstrate the classic presentation of a lucid interval between the initial trauma and subsequent neurological deterioration.
• Following injury, the patient may or may not lose consciousness. If he or she becomes unconscious, the patient may awaken or remain unconscious.
• Severe headache
• Vomiting
• Seizure
• Patients with posterior fossa EDH may have a dramatic delayed deterioration. The patient can be conscious and talking and a minute later apneic, comatose, and minutes from death.

Physical

• Cushing response, consisting of the following, can indicate increased ICP:
  • Hypertension
  • Bradycardia
  • Bradypnea
• Level of consciousness may be decreased, with decreased or fluctuating GCS.
• Contusion, laceration, or bony step-off may be observed in the area of injury.
• Dilated, sluggish, or fixed pupil(s), bilateral or ipsilateral to injury, suggest increased ICP or herniation.
• Classic triad indicating transtentorial herniation consists of the following:
  • Coma
  • Fixed and dilated pupil(s)
  • Decerebrate posturing
• Hemiplegia contralateral to injury with herniation may be observed.

Causes

• EDH results from traumatic head injury, usually with an associated skull fracture and arterial laceration.

Fluid Therapy (مایع درمانی)

Fluid Therapy

Maintenance

Weight (kg)	Addn. Maintenance	Total Hourly Maintenance
0 - 10 kg	4 ml/kg/hr	4 ml/kg/hr
10 - 20 kg	2 ml/kg/hr	40 ml/hr + 2 ml/kg/hr (>10 kg)
> 20 kg	1 ml/kg/hr	60 ml/hr + 1 ml/kg/hr (>20 kg)

Special considerations:

Increase by 12% / degree C of fever
First day of life:

less than 32 weeks or les than 1 kg = 4 ml/kg/hr
otherwise = 3 ml/kg/hr

Glucose-containing fluids should only be used as maintenance, not volume replacement.

NPO Deficit

Calculate: Deficit = Maintenance x hours NPO
Traditional: Replace during the surgery with

_ in 1st hour
_ in 2nd hour
_ in 3rd hour

Do not use glucose-containing fluids.

More aggressive, especially for DSU patients, replace _ in first 30 minutes, rest in remaining time during surgery.

Intraoperative Third Space Loss

Simple	no extra fluid.
Moderate (simple laparotomy)	2-5 mls/kg/hr
Major (large visceral exposure)	5-10 mls/kg/hr
Extreme (above + multiple resections)	10-15 mls/kg/hr
Necrotizing enterocolitis	50-100 mls/kg/hr!

Do not use glucose-containing fluids.

 

 

 

ALLOWABLE BLOOD LOSS (ABL)

ABL = Estimated Blood Volume X	(Starting Hct - Acceptable Hct)
	Starting Hct

Estimated blood volume

in non-obese patients, in ml/kg

Premature newborn	90 - 100 ml/kg
Full-term newborn	80 - 90
3 - 12 months	75 - 80
3 - 6 years	70 - 75
> 6 years	65 - 70

Hematocrits in healthy patients

	Normal Hematocrit		Acceptable Hematocrit
	mean	range
Premature newborn	45	40-60	35-40
Term newborn	54	45-70	35-40
3 months*	36	28-42	25
1 year	38	34-42	20-25
6 years	38	35-43	20-25

 

Remember, anemia at approx. 3 months is physiological reflecting the falling HbF and rising HbA. The P50 may be as high as 32.

Other

PRBC's have a hematocrit of approximately 70.

Once exposed to a unit of PRBC's, a patient should receive as much of the unit as safely possible.

Try and calculate anticipated values preoperatively to avoid the distraction of intra-op calculations.

BLOOD AND COMPONENT THERAPY

General Comments

Fluid Bolus = 10 ml/kg
Resuscitative Fluid Bolus = 20 ml/kg
Break FFP and PRBC into "Pedi Packs" of 10-20 ml/kg when patient less than 15 kg -- to conserve blood products and minimize exposure to additional donors

Specific Components

 

Citrated PRBC

Hct @ 70%
10 ml/kg PRBC = in adults to 1 unit PRBC
"one unit" increases Hct by 3%

FFP

> 70% of fresh procoagulant factors
high in citrate

Cryoprecipitate

(0.3 unit/kg)
50% of factor VIII
20-40% of fibrinogen and some factor XIII

Administer through standard blood filter for hemophilia A, von Willebrand's dz, hypofibrinogenemia and DIC. Exists in concentrated form (10:1 volume ratio)

Platelets

0.1 - 0.3 units/kg will usually cause platelet count to rise by 20-70,000/mm3
use standard blood administration filter
FFP also in the fluid

Problems with Massive Transfusions

If whole blood were available, clinical bleeding might not be seen with 3 blood volume "exchanges". With component therapy it is seen earlier.

Dilutional Clotting Factor Coagulopathy

Likely to occur when blood loss > 1.5 blood volumes.
Correlates with PT + PTT prolonged > 1.5 control, which is the approximate threshold to treat.

Dilutional thrombocytopenia

Clinical bleeding correlates with a platelet count £ 50,000/min3, thus the starting count is crucial. If PRBC's and FFP are used to replace losses, then the platelet count will be approximately

70% of baseline at one volume exchanges
40% of baseline at two volume exchanges
20% of baseline at three volume exchanges

Citrate toxicity (ionized hypocalcemia)

More likely when FFP given > 1 ml/kg/min, especially through a CVP line.

Calcium

frequent small doses are better than large boluses Ca Chloride 0.1 ml/kg or 2.5 mg/kg, through central lines Ca Gluconate 1 ml/kg or 7.5 mg/kg, through PIV

Hyperkalemia

Avoid hyperventilation Arrhythmias worse with hypocalcemia

BLOOD PRODUCT COMPOSITION

Citrated Citrated Whole blood PRBC	Normal	Citrated Whole Blood	Citrated PRBC	FFP
pH	7.4	~6.8	~6.8	~6.8
PCO2	40	~190	~190	~190
Base deficit mEq/L	0	~12	~12	~12
K+ (mEq/L)	3.5-5.0	> 18	> 18	4-8
Citrate	---	++	+	+++
Factors V & VIII	Normal	less than20%	---	80-100%
Fibrinogen	Normal	---	---	---
Platelets	160-400K	---	---	---
2-3 DPG	Normal	3%	3%	---
Hct	35-45	35-45	70-80	---
Temperature [infinity]C	37	1-6	1-6	Cold

Normal screening tests

	Pre-Term Newborn		Newborn	Adult
Test	< 1500 gm	1500-2000gm	Full-Term
Platelet count (x103/mm3)	250 (>150)	250 (>150)	250 (>150)	300 (>150)
PTT (secs)	108 (<150)	80 (<120)	65 (<84)	44 (<50)
PT (secs)	17 (<20)	16 (<19)	13.5 (<16)	12 (<14)
Thrombin time (secs)	15 (<20)	15 (<20)	14 (<18)	10 (<12)

 

Effects of anesthesia on the heart

PROVIDENCE, R.I. – Researchers at Rhode Island Hospital have created the first animal model that can reveal the side effects of anesthetic agents (the substances used to block pain during surgery) in individuals genetically predisposed to sudden cardiac death. The researchers also found that some anesthetic agents may trigger arrhythmias. The study appears in an upcoming issue of the American Journal of Physiology – Heart Circulation Physiology and is currently available online.

Researchers know that genetic mutations can predispose individuals to arrhythmia and/or sudden cardiac death (SCD), a leading cause of death in the United States. Between one in 2,500 and one in 5,000 individuals are born with mutations that cause long QT syndrome (LQTS), a disorder of the heart's electric system, and a determining factor in the development of arrhythmia and/or SCD. Ninety percent of the known mutations cause loss of function of ion channels responsible for LQTS types 1 and 2 (LQT1 and LQT2).

LQTS leads to a prolonged QT interval on electrocardiograms. The QT interval refers to the time it takes the chambers of the heart to "repolarize" themselves so that the heart is ready for another contraction cycle. When this timeframe is lengthened, it is associated with triggering irregular arrhythmia that can cause sudden cardiac arrest.

Earlier this year, researchers at the Cardiovascular Research Center at Rhode Island Hospital developed a first-of-its-kind genetic animal model to study arrhythmia and SCD that mirrors what happens in individuals who have mutations of the LQT1 or LQT2 genes. With the rising interest in pharmacogenomics (the study of the effect of an individual's genotype on the body's potential response to medications) the researchers have taken the model one step further and have developed what they believe is the first model to test the safety and efficacy of drugs such as anesthetics when these genetic mutations are present.

Senior author Gideon Koren, MD, director of the Cardiovascular Research Center at Rhode Island Hospital and a professor of medicine at the Warren Alpert Medical School of Brown University, says, "We believe the animal model we have created is the first to be able to accurately predict the effects of various anesthetic agents when LQTS is present. Also, our findings indicate that some anesthetic agents can trigger arrhythmias."

The researchers looked at five common anesthetic agents, including isoflurane, thiopental, midazolam, propofol and the veterinary anesthetic ketamine. Varied effects were noted with each anesthetic in the different models. For instance, isoflurane resulted in a prolonged QT interval in LQT2 but not in LQT1 models, whereas thiopental prolonged the QT interval in both LQT1 and LQT2, though the increase was less pronounced in LQT1. Midazolam prolonged the QT duration in both LQT1 and LQT2 but not in controls, while propofol significantly increased the QT interval in both LQT1 and LQT2 models and the control group.

During the monitoring periods under anesthesia, signs of altered repolarization and arrhythmias were noted only in LQT2 models. Multiple premature ventricular contractions, which can have a marked effect in humans, occurred in many LQT2 models under midazolam, ketamine or thiopental. Also noted is that isoflurane and propofol were especially proarrhythmic in LQT2 models and led to sudden cardiac death in a total of three LQT2 out of nine LQT2 models.

Koren concludes, "We anticipate a great deal more in the way of findings from the development of this model. For now, this study should serve as a reminder to anesthesiologists that an ECG prior to surgery must be carefully studied." He adds, "Further, we would recommend that for those individuals whose ECG appears borderline for LQTS, genotyping may be advisable in order to determine if there is a mutation of the LQT1 or LQT2 genes before selecting anesthetic agents."

Anesthesia

 

If you are having surgery, your doctor will give you a drug called an anesthetic. Anesthetics reduce or prevent pain. There are four main types.

Local: numbs one small area of the body. You stay awake and alert.

• Conscious or intravenous (IV) sedation: uses a mild sedative to relax you and pain medicine to relieve pain. You stay awake but may not remember the procedure afterwards.
• Regional anesthesia: blocks pain in an area of the body, such an arm or leg. Epidural anesthesia, which is sometimes used during childbirth, is a type of regional anesthesia.
• General anesthesia: affects your whole body. You go to sleep and feel nothing. You have no memory of the procedure afterwards.

The type of anesthesia your doctor chooses depends on many factors. These include the procedure you are having and your current health