T4 on the beach how many stages

Before ambulation, women should be observed for 30 minutes after intrathecal or epidural drug administration to assess maternal and fetal well-being.

A recent study indicated that the early administration of CSE analgesia to nulliparous women did not increase the cesarean section delivery rate. Intrathecal injection of fentanyl 10—25 mcg or sufent-anil 5—10 mcg alone or, more commonly, with 1 mL isobaric bupivacaine 0.

The most common side effects of intrathecal opioids are pruritus, nausea, vomiting, and urinary retention. Rostral spread resulting in delayed respiratory depression is rare with fentanyl and sufentanil and usually occurs within 30 minutes of injection.

Transient nonreassuring fetal heart rate patterns may occur because of uterine hyperstimulation, presumably as a result of a rapid decrease in maternal catecholamines resulting in the unopposed effects of oxytocin. The incidence of fetal heart rate abnormalities may be greater in multiparous woman with a rapidly progressing, painful labor.

Most studies have demonstrated that the incidence of emergency cesarean section delivery is no greater with CSE analgesia than after conventional epidural analgesia. Postdural puncture headache is always a risk after intrathecal injection.

However, the incidence of headache is no greater with CSE analgesia compared with standard epidural analgesia. Unintentional intrathecal catheter placement through the dural puncture site is also rare after use of a gauge spinal needle for CSE analgesia.

The potential exists for epidurally administered drug to leak intrathecally through the dural puncture, particularly if large volumes of drug are rapidly injected.

The patient may have a partial block insufficient for surgery with an epidural that may or may not work. An algorithm for patient management in the event of an incomplete epidural is presented in Figure 5.

Although paracervical block effectively relieves pain during the first stage of labor, it is now rarely used in the United States because of its association with a high incidence of fetal bradycardia, particularly with the use of bupivacaine. This may be related to uterine artery constriction or increased uterine tone.

The use of levobupivacaine compared to racemic bupivacaine has been demonstrated to result in fewer fetal bradycardias. Paracervical block is a useful technique to provide analgesia for uterine curettage. The technique is very simple and involves a submucosal injection of local anesthetic at the vaginal fornix near the neural fibers innervating the uterus Figure 6.

Paravertebral lumbar sympathetic block is a reasonable alternative to central neuraxial blockade. Lumbar sympathetic block effectively interrupts the painful transmission of cervical and uterine impulses during the first stage of labor. Leighton et al. However, there was no difference in the rate of dilatation during the active phase of labor.

Although there is less risk of fetal bradycardia with lumbar sympathetic block compared with paracervical blockade, technical difficulties associated with the performance of the block and risks of intravascular injection have hampered its routine use.

Hypotension may also occur with lumbar sympathetic blocks. The pudendal nerves are derived from the lower sacral nerve roots S2—4 and supply the vaginal vault, perineum, rectum, and sections of the bladder.

The nerves are easily blocked transvaginally where they loop around the ischial spines. A recent study demonstrated that a pudendal nerve block does not provide reliable analgesia for the second stage of labor, probably related to the upper vagina being innervated by lumbar, rather than sacral, fibers.

However, the block is useful for episiotomy and repair. There may also be post-partum benefits of pudendal nerve block. For instance, a unilateral nerve stimulator—guided pudendal nerve block with ropivacaine was associated with decreased pain and less need for supplemental analgesia during the first 48 hours after the performance of mediolateral episiotomy at vaginal delivery.

The most common indications for cesarean section delivery include failure to progress, nonreassuring fetal status, cephalopelvic disproportion, malpresentation, prematurity, and prior uterine surgery involving the corpus. The choice of anesthesia should depend on the urgency of the procedure in addition to the condition of the mother and fetus. Before the initiation of any anesthetic technique, resuscitation equipment for mother and neonate should be made available Table 2.

A survey of obstetric anesthesia practices in the United States demonstrated that most patients undergoing cesarean section delivery do so under spinal or epidural anesthesia.

Regional techniques have several advantages: They reduce the risk of gastric aspiration, avoid the use of depressant anesthetic drugs, and allow the mother to remain awake during delivery. Operative blood loss may also be reduced with regional compared with general anesthesia. Generally speaking, with regional techniques, the duration of antepartum anesthesia does not affect neonatal outcome, provided that there is no protracted aortocaval compression or hypotension.

The risk of hypotension may be greater than during vaginal delivery because the sensory block must extend to at least the T4 dermatome. Studies have shown preloading with crystalloid does not reliably prevent neuraxial anesthesia—induced hypotension. In fact, recent studies indicate that intravenous co-loading at the time of intrathecal injection is as effective as prehydrating before neuroblockade.

If hypotension occurs despite these measures, left uterine displacement should be increased, the rate of IV infusion augmented, and IV ephedrine 5—15 mg or phenylephrine 25—50 mcg administered incrementally. The greatest success in preventing hypotension has been found with a continuous low-dose infusion of phenylephrine until delivery.

Subarachnoid block is probably the most commonly adminis-tered regional anesthetic for cesarean section delivery because of its speed of onset and reliability. It has also become an alternative to general anesthesia for emergency cesarean section.

However, bupivacaine has now become the most widely used drug for spinal anesthesia for cesarean delivery. Using 0. Recent studies using spinal ropivacaine have shown less hypotension and faster recovery but a slower onset compared to bupivacaine. However, it has been questioned whether ropivacaine produces spinal anesthesia of similar quality to that of bupivacaine. Hemodynamic monitoring during cesarean section should be similar to that used for other surgical procedures, with the exception that blood pressure should be monitored at a minimum of every 3 minutes before the birth of the baby.

Before delivery, oxygen should be routinely administered to optimize fetal oxygenation. Table 3 lists local anesthetics and the dosages commonly used for cesarean section delivery with subarachnoid block. Despite an adequate dermatomal level, women may experience varying degrees of visceral discomfort, particularly during exteriorization of the uterus and traction on abdominal viscera. Improved perioperative analgesia can be provided by the addition of fentanyl 20 mcg or preservative-free morphine 0.

Preservative-free morphine produces significant analgesia in doses ranging from 0. Higher doses of spinal morphine result in greater pruritus. Delayed respiratory depres-sion can occur with spinal morphine but is extremely rare and more often associated with comorbid conditions such as obesity.

The respiratory depression is due to the rostral spread of subarachnoid morphine. In a retrospective study of parturients receiving spinal morphine 0. In addition, spinal clonidine, in doses of 60 to mcg, improves intraoperative analgesia and decreases shivering in women undergoing cesarean delivery.

However, hypotension and sedation have been reported with spinal clonidine and may limit its routine use. Nausea and vomiting may be alleviated by the administration of ondansetron or metoclopramide. Maternal sedation should be avoided if possible. If the initial block is not adequate, concern exists regarding a repeat spinal injection and the potential for inadvertent high spinal anesthetic. See Figure 5 for a range of options available in situations in which spinal anesthesia fails to prove adequate for surgery.

Epidural anesthesia has a slower onset of action and a larger drug requirement to establish an adequate sensory block compared with spinal anesthesia. The advantages are a perceived reduced risk of postdural puncture headache and the ability to titrate the local anesthetic through the epidural catheter. However, correct placement of the epidural catheter and avoidance of inadvertent intrathecal or intravascular injection are essential.

A small dose of local anesthetic, lidocaine 45 mg or bupivacaine 5 mg, produces a readily identifiable sensory and motor block if injected intrathecally. However, a recent study has suggested that ropivacaine 15 mg was not a useful intrathecal test dose because a slow onset of motor blockade may preclude the timely diagnosis of intrathecal injection. The addition of epinephrine 15 mcg with careful continuous heart rate and blood pressure monitoring may herald intravascular injection with a transient increase in heart rate and blood pressure.

However, an epinephrine test dose is not reliable because false-positive results do occur in the form of tachycardia related to painful uterine contractions. In addition, epinephrine may potentially reduce uteroplacental perfusion in some patients. Electrocardiography and the application of a peak-to-peak heart rate criterion may improve detection 10 beats over maximum heart rate preceding epinephrine injection.

Rapid injection of 1 mL of air with simultaneous precordial Doppler monitoring appears to be a reliable indicator of intravascular catheter placement. Most important, a negative test, although reassuring, does not eliminate the need for the fractional administration of local anesthetic.

Adequate anesthesia can be usually achieved with 15—25 mL of local anesthetic given in divided doses. The patient should be monitored as with spinal anesthesia. Because of its extremely high rate of metabolism in maternal and fetal plasma, 2-chloroprocaine provides a rapid-onset, reliable block with minimal risk of systemic toxicity. It is the local anesthetic of choice in the presence of fetal acidosis and when a preexisting epidural block is to be rapidly extended for an urgent cesarean section delivery.

Neurologic deficits after massive inadvertent intrathecal administration of the drug have occurred with the formulation containing a relatively high concentration of sodium bisulfite at a low pH. However, severe spasmodic back pain has been described after epidural injection of large volumes of Nesacaine-MPF in surgical patients, but not in parturients. This has been attributed to an EDTA-induced leaching of calcium from paravertebral muscles.

The most recent formulation of 2-chloroprocaine contains no additives and is packaged in an amber vial to prevent oxidation.

Bupivacaine 0. Considerable attention has been focused on the drug because it was reported that unintentional intravascular injection could result not only in convulsions but also in almost simultaneous cardiac arrest, with patients often refractory to resuscitation.

The greater cardiotoxicity of bupivacaine and etidocaine compared with other amide local anesthetics has been well established. When using potent long-acting amide local anesthetics, fractioning the induction dose is critical. Lidocaine has an onset and duration intermediate to those of 2-chloroprocaine and bupivacaine. The need to include epinephrine in the local anesthetic solution to ensure adequate lumbosacral anesthesia limits the use of lidocaine in women with maternal hypertension and uteroplacental insufficiency.

Prolonged postoperative pain relief can be provided by the epidural administration of an opioid, such as morphine 4 mg, or the use of PCEA.

Delayed respiratory depression may occur with the use of morphine; hence, the patient must be monitored carefully in the postoperative period. Recently, a lipid-encapsulated preparation of morphine DepoDur has been approved for post—cesarean section delivery analgesia. It can be used only epidurally, can last up to 48 hours, and the patient must be monitored for delayed respiratory depression.

A potential limitation in obstetrics is that once the drug is administered, additional local anesthetic cannot be injected epidurally for a period of up to one hour since the local anes-thetic may cause an uncontrolled release of morphine from the lipid.

Carvalho et al. No significant side effects were observed. Another study showed lower pain scores and fewer supplemental analgesia requirements for patients receiving extended-release morphine compared to preservative-free morphine. No differences in nausea, pruritus, or sedation scores were observed. In addition, the bolus administration of epidural fentanyl 50— mcg has been found to result in activity at both spinal and supraspinal sites of action and to improve the quality of anesthesia.

A study of anesthesia-related deaths in the United States between and showed that the case fatality rate with general anesthesia was Most anesthesia-related deaths were a result of cardiac arrest due to hypoxemia when difficulties securing the airway were encountered. Pregnancy-induced anatomical and physiological changes, such as reduced FRC, increased oxygen consumption, and oropharyngeal edema may expose the patient to serious risks of desaturation during periods of apnea and hypoventilation.

The risk of the inhalation of gastric contents is increased in pregnant women, particularly if difficulty is encountered estab-lishing an airway or if airway reflexes are obtunded. Measures to decrease the risks of aspiration include comprehensive airway evaluation, prophylactic administration of nonparticulate antacids, and the preferred use of regional anesthesia. If aspiration occurs, management includes immediate treatment of hypoxemia with continuous positive airway pressure CPAP and possible rigid bronchoscopy.

Recent studies do not support the administration of corticosteroids or lung lavage with saline and bicarbonate to neutralize acidity. Prophylactic antibiotics are not recommended because gastric contents are sterile. Regional anesthesia may be associated with hypotension, which is related to the degree and rapidity of local anesthetic—induced sympatholysis. Thus, greater hemodynamic stability may be observed with epidural anesthesia, where gradual titration of local anesthetic allows for better control of the block level as well as for adequate time for vasopressor administration in anticipation of blood pressure reduction.

The risk of hypotension is lower in laboring women compared with nonlaboring women. It has been demonstrated that for effective prevention of hypotension, the blood volume increase from preloading must be sufficient to result in a significant increase in cardiac output.

This was possible only with the administration of hetastarch 0. Nonetheless, controversy exists regarding the efficacy of volume loading in the prevention of hypotension. A recent study using a prophylactic phenylephrine infusion combined with a rapid crystalloid co-loading given at the time of intrathecal injection markedly reduced the incidence of spinal anesthesia—induced hypotension.

If hypotension does occur despite prehydration, therapeutic measures should include increasing the displacement of the uterus, rapid infusion of IV fluids, titration of IV ephedrine 5—10 mg , and oxygen administration. In the presence of maternal tachycardia, phenylephrine 25—50 mcg may be substituted for ephedrine in women with normal uteroplacental function. Continued vigilance and active management of hypotension can prevent serious sequelae in both mother and neonate.

High, or total, spinal anesthesia is a rare complication of intrathe-cal injection in modern-day practice. It occurs with an excessive cephalad spread of local anesthetic in the subarachnoid space. Unintentional intrathecal administration of epidural medication as a result of dural puncture or catheter migration may also result in this complication. Left uterine displacement and continued fluid and vasopressor administration may be necessary to achieve hemodynamic stability.

The reverse Trendelenburg position does not prevent cephalad spread and may cause cardiovascular collapse because of venous pooling related to sympathectomy. Rapid control of the airway is essential, and endotracheal intubation may be necessary to ensure oxygenation without aspiration. Unintended intravascular injection or drug accumulation after repeated epidural injection can result in high serum levels of local anesthetic. Rapid absorption of local anesthetic from highly vascular sites of injection may also occur after paracervical and pudendal blocks.

Resuscitation equipment should always be available when any major nerve block is undertaken. IV access, airway equipment, emergency drugs, and suction equipment should be immediately accessible. To avoid systemic toxicity of local anesthetic agents, strict adherence to recommended dosages and avoidance of unintentional intravascular injection are essential. Despite these precautions, life-threatening convulsions and, more rarely, cardiovascular collapse may occur.

Seizure activity has been treated with IV thiopental 25—50 mg or diazepam 5—10 mg. In current clinical practice, propofol 20—50 mg or midazolam 2—4 mg is more commonly used. The airway should be evaluated and oxygenation main-tained. In a case report, lipid emulsion was used to treat refractory cardiac arrest resulting from bupivacaine toxicity.

The mechanism of action is unclear but may result from the greater affinity of bupivacaine for the lipid or because the lipid provides a substrate for a bupivacaine-poisoned mitochondrial energy system. Further study is required to deter-mine the efficacy of this treatment. However, it would seem prudent that treatment of a pregnant woman intoxicated with bupivacaine should include the administration of lipid emulsion early on in the resuscitation. The early administration of lipid has also been shown to prevent progression to cardiac arrest when bupivacaine was injected intravascularly.

Whenever there is maternal cardiac arrest, regardless of cause, the fetus should be delivered early on, usually within 5 minutes, if attempts at resuscitation are unsuccessful in relieving aortocaval compression and ensuring the efficiency of cardiac massage. Pregnant women have a higher risk of developing a postdural puncture headache PDPH should an inadvertent dural puncture occur. In a recent meta-analysis, the risk of PDPH was The reduced epidural pressure increases the risk of cerebrospinal fluid leakage through the dural opening.

Russell et al. The incidence of headache was higher with the use of a gauge compared to an gauge epidural needle. The pathophysiology and management of postdural puncture headache are discussed in greater detail in Postdural Puncture Headache.

Neurologic sequelae of central neuraxial blockade, although rare, have been reported. Pressure exerted by a needle or catheter on spinal nerve roots produces immediate pain and necessitates repositioning.

Infections such as epidural abscess and meningitis are very rare and may be a manifestation of systemic sepsis. In recent years, several cases of epidural abscess have been reported after epidural catheterization in obstetric patients.

Potential risk factors identified from these cases are entry-point infections from usual causative organisms eg, Staphylococcus aureus , possible systemic sources of infection, poor aseptic technique, and prolonged catheterization. Epidural hematoma can also occur, usually in association with coagulation defects. However, epidural hematoma may also occur spontaneously, unrelated to instrumentation.

The pathogenesis may be due to a weakened epidural vascular architecture. Nerve root irritation may have a protracted recovery, lasting weeks or months. Peripheral nerve injury as a result of instrumentation, lithotomy position, or compression by the fetal head may occur even in the absence of neuraxial technique.

Pregnancy and parturition are considered high risk when accompanied by conditions unfavorable to the well-being of the mother or fetus, or both. Maternal problems may be related to the pregnancy; that is, preeclampsia-eclampsia, hypertensive disorders of pregnancy, or antepartum hemorrhage resulting from placenta previa or abruptio placentae.

Diabetes mellitus; cardiac, chronic renal, and neurologic problems; sickle cell disease; asthma; obesity; and drug abuse are not related to pregnancy but often are affected by it.

Prematurity gestation of less than 37 weeks , postmaturity gestation of 42 weeks or longer , intrauterine growth retardation, and multiple gestation are fetal conditions associated with risk. During labor and delivery, fetal malpresentation eg, breech, transverse lie , placental abruption, compression of the umbilical cord eg, prolapse, nuchal cord , precipitous labor, or intrauterine infection eg, prolonged rupture of membranes may increase the risk to the mother or fetus.

In general, the anesthetic management of the high-risk parturient is based on the same maternal and fetal considerations as for the management of healthy mothers and fetuses. However, there is less room for error because many of these functions may be compromised before the induction of anesthesia.

The added appearance of convulsions is diagnostic for eclampsia. Preeclampsia-eclampsia is a disease unique to humans, occurring predominantly in young nulliparous women. Symptoms usually appear after the twentieth week of gestation, occasionally earlier with a hydatidiform mole. Delivery of the infant and placenta is the only effective treatment; as a result, preeclampsia is a leading cause of iatrogenic preterm delivery in developed countries.

The origin of preeclampsia-eclampsia is unknown, but all patients manifest placental ischemia. Decreased placental per-fusion occurs in early pregnancy in women destined to become preeclamptic, and there is a failure of the normal trophoblastic invasion.

In normal pregnancy, the diameter of spiral arteries increase approximately four-fold to create flaccid tubes that provide a low-resistance pathway to the intervillous space. This angiogenesis is a result of the trophoblast invasion into the decidual and myometrial segments of the spiral arteries. However, in preeclamptic women, the myometrium is not invaded.

This causes superficial placental implantation, resulting in decreased placental perfusion and ischemia related to stiff, muscular spiral arteries. Placental ischemia results in a release of uterine renin, an increase in angiotensin activity, and a widespread arteriolar vasoconstriction causing hypertension, tissue hypoxia, and endothelial damage Figure 7.

The fixation of platelets at sites of endothelial damage results in coagulopathies, occasionally in disseminated intravascular coagulation. Enhanced angioten-sinmediated aldosterone secretion leads to increased sodium reabsorption and edema. Proteinuria, a sign of preeclampsia, is also attributed to placental ischemia, which leads to local tissue degeneration and a release of thromboplastin with subsequent deposition of fibrin in constricted glomerular vessels.

As a result, an increased permeability to albumin and other plasma proteins occurs. Furthermore, there is a decreased production of prostaglandin E, a potent vasodilator secreted in the trophoblast, which normally balances the hypertensive effects of the rennin—angiotensin system. Many of the symptoms associated with preeclampsia, including placental ischemia, systemic vasoconstriction, and increased platelet aggregation, may result from an imbalance between the placental production of prostacyclin and thromboxane.

During normal pregnancy, the placenta produces equal amounts of the two, but in a preeclamptic pregnancy, there is seven times more thromboxane than prostacyclin. According to the latest theory, endothelial cell injury is central to the development of preeclampsia.

This injury occurs as a result of reduced placental perfusion, leading to a production and release of substances possibly lipid peroxidases causing endothelial cell injury. Abnormal endothelial cell function contributes to an increase in peripheral resistance and other abnormalities noted in preeclampsia through a release of fibronectin, endothelin, and other substances. In rodent models, two placental antiangiogenic proteins have been identified and likely play a role in the pathogenesis of preeclampsia.

Soluble fms-like tyrosine kinase-1 sFlt-1 is upregulated in the placenta of preeclamptic women. Levine et al. Another antiangiogenic protein, soluble endoglin sEng , is elevated in cases of HELLP syndrome which consists of hemolysis, elevated liver enzymes, and low platelet count.

In severe preeclampsia-eclampsia, all major organ systems are affected because of widespread vasospasm. Global cerebral blood flow is not diminished, but focal hypoperfusion cannot be ruled out. Postmortem examination has revealed hemorrhagic necrosis in the proximity of thrombosed precapillaries, suggesting intense vasoconstriction.

Edema and small foci of degeneration have been attributed to hypoxia. Petechial hemorrhages are common after the onset of convulsions.

Symptoms related to the above changes include headache, vertigo, cortical blindness, hyperreflexia, and convulsions. Heart failure may occur in severe cases as a result of peripheral vasoconstriction and increased blood viscosity from hemoconcentration. Decreased blood supply to the liver may lead to periportal necrosis of variable extent and severity. Subcapsular hemorrhages account for the epigastric pain encountered in severe cases.

In the kidneys, there is swelling of glomerular endothelial cells and deposition of fibrin, leading to a constriction of the capillary lumina. Renal blood flow and glomerular filtration rate decrease, resulting in reduced uric acid clearance and, in severe cases, increase in creatinine.

Although preeclampsia is accompanied by exaggerated retention of water and sodium, the shift of fluid and proteins from the intravascular into the extravascular compartment may result in hypovolemia, hypoproteinemia, and hemoconcentration, which may be further aggravated by proteinuria. The risk of uteroplacental hypoperfusion and poor fetal outcome correlates with the degree of maternal plasma and protein depletion.

The prolongation of prothrombin and partial thromboplastin times indicates a consumption of procoagulants. The HELLP syndrome is a particular form of severe preeclampsia characterized by hemolysis, elevated liver enzymes, and low platelets. The goals of the management of the patient with preeclamp-sia-eclampsia are to prevent or control convulsions, improve organ perfusion, normalize blood pressure, and correct clotting abnormalities.

The mainstay of anticonvulsant therapy in the United States is magnesium sulfate. Its efficacy in preventing seizures has been well substantiated, but its mechanism of action remains controversial. Antihypertensive therapy in preeclampsia is used to lessen the risk of cerebral hemorrhage in the mother while maintaining, or even improving, tissue perfusion.

There is no evidence to suggest that antihypertensive therapy delays disease progression or improves perinatal outcome. Plasma volume expansion combined with vasodilation fulfills these goals. Hydralazine is the most commonly used vasodilator because it increases uteroplacental and renal blood flows. However, side effects include tachycardia, palpitations, headache, and neonatal thrombocytopenia.

Nitroprusside is used during laryngoscopy and intubation to prevent dangerous elevations in blood pressure. Trimethaphan, a ganglion blocking agent, is useful in hypertensive emergencies when cerebral edema and increased intracranial pressure are a concern because it does not cause vasodilation in the brain.

Consumption coagulopathy may require infusion of fresh whole blood, platelet concentrates, fresh frozen plasma, and cryoprecipitate. Delivery is indicated in refractory cases or if the pregnancy is close to term.

In severe cases, aggressive management should continue for at least 24—48 hours after delivery. There are very few contraindications for epidural anesthesia in labor and delivery. In the presence of severe clotting abnormalities or severe plasma volume deficit, the risk—benefit ratio favors other forms of anesthesia.

In volume-depleted patients positioned with left uterine displacement, epidural anesthesia does not cause an unacceptable reduction in blood pressure and leads to a significant improvement in placental perfusion. The total maternal body clearance of amide local anesthetics is prolonged in preeclampsia, and repeated administration of these drugs can lead to higher blood concentrations than in normotensive patients. For cesarean section delivery, the sensory level of regional anesthesia must extend to T3—4, making adequate fluid therapy and left uterine displacement even more vital.

Epidural anesthesia has been preferred to spinal anesthesia in preeclamptic women because of its slower onset of action and controllability. In the past, the rapid onset of sympathectomy related to spinal anesthesia was associated with hypoten-sion, particularly in volume-depleted patients. However, in two recent studies, the incidence of hypotension, perioperative fluid and ephedrine administration, and neonatal conditions were found to be similar in preeclamptic women who received either epidural or spinal anesthesia for cesarean delivery.

Aya et al. There is an increased sensitivity to vasopressors in preeclampsia; therefore, lower doses of ephedrine and phenylephrine are usually required to correct hypotension. Antepartum hemorrhage occurs most commonly in association with placenta previa abnormal placental implantation on the lower uterine segment and partial to total occlusion of the internal cervical os and abruptio placentae.

Placenta previa occurs in 0. It may be associated with abnormal fetal presenta-tion, such as transverse lie or breech. Placenta previa should be suspected whenever a patient presents with painless, bright red vaginal bleeding, usually after the seventh month of pregnancy. The diagnosis is confirmed by ultrasonography. Unless the lowest placental edge is more than 2 cm from the internal cervical os, an abdominal delivery is usually required.

If the bleeding is not profuse and the fetus is immature, obstetric management is conservative to prolong the pregnancy. In severe cases or if the fetus is mature at the onset of symptoms, prompt delivery is indicated, usually by cesarean section. An emergency hysterectomy may be required because of severe hemorrhage, even after the delivery of the placenta, because of uterine atony.

In patients who have undergone prior uterine surgery, particularly prior cesarean delivery, the risk of severe hemorrhage is even greater, owing to a higher incidence of placenta acreta penetration of the myometrium by placental villi. Abruptio placentae occurs in 0. Complications include Couvelaire uterus which occurs when extravasated blood dissects between the myometrial fibers , renal failure, disseminated intravascular coagulation, and anterior pituitary necrosis ie, Sheehan syndrome.

The maternal mortality is high 1. The diagnosis of abruptio placentae is based on the presence of uterine tenderness, hypertonus, and vaginal bleeding of dark, clotted blood. Bleeding may be concealed if the placental margins have remained attached to the uterine wall. Changes in maternal blood pressure and pulse rate, indicative of hypovolemia, may occur if the blood loss is severe. Fetal movements may increase during acute hypoxia and decrease if hypoxia is gradual.

Fetal bradycardia and death may ensue. The establishment of invasive monitoring arterial line, central venous catheter and blood volume replacement via a or gauge catheter is usually required. If clotting abnormalities exist, blood components and fresh frozen plasma, cryoprecipitate, and platelet concentrates may be required. The choice of anesthetic for a woman with placental abruption depends on maternal and fetal condition and how urgently the procedure needs to be performed.

General anesthesia is indicated in the presence of uncontrolled hemorrhage and coagulation abnormalities. Epidural anesthesia may be used, particularly if there is a functioning epidural in place during labor at the time of abruption and there is no hemodynamic instability. Vincent et al. However, this was uncorrected hypotension, which, with intravascular fluid replacement hemodynamics, returned to normal even with epidural anesthesia.

Preterm labor and delivery present a significant challenge to the anesthesiologist because both the mother and the infant may be at risk. The definition of prematurity was altered to distinguish between the preterm infant, born before the thirty-seventh week of gestation, and the small-for-gestational-age infant, who may be born at term but whose weight is more than 2 standard deviations below the mean.

Severe complications, such as respiratory distress syndrome, intracranial hemorrhage, hypoglycemia, hypocalcemia, and hyperbilirubinemia, are prone to develop in preterm infants. Obstetricians frequently try to inhibit preterm labor to obtain time for fetal lung maturity. Delaying delivery by even 24—48 hours may be beneficial if glucocorticoids are administered to the mother to enhance fetal lung maturity.

Numerous maternal complications, including hypotension, hypokalemia, hyperglycemia, myocardial ischemia, pulmonary edema, and death, have been reported as a result of these tocolytics. Complications may occur because of interactions with anes-thetic drugs and techniques. The premature infant is known to be more vulnerable than the term newborn to the effects of drugs used in obstetric analgesia and anesthesia.

However, there have been few systemic studies to determine the maternal and fetal pharmacokinetics and dynamics of drugs throughout gestation.

There are several postulated causes of enhanced drug sensi-tivity in the preterm newborn: less protein available for drug binding; higher levels of bilirubin, which may compete with the drug for protein binding; greater drug access to the central nervous system because of a poorly developed blood—brain barrier; greater total body water and lower fat content; and a decreased ability to metabolize and excrete drugs.

In selecting the anesthetic drugs and techniques for delivering a preterm infant, concerns regarding drug effects on the newborn are far less important than preventing asphyxia and trauma to the fetus.

For vaginal delivery, well-conducted epidural anesthesia is advantageous in providing good perineal relaxation. Before induction of epidural blockade, the anesthesiologist should ascertain that the fetus is neither hypoxic nor acidotic. Asphyxia results in a redistribution of fetal cardiac output, which increases oxygen delivery to vital organs such as the brain, heart, and adrenals.

Regardless, these changes in the preterm fetus may be better preserved with bupivacaine or chloroprocaine than with lidocaine. Preterm infants with breech presentation are usually delivered by cesarean section. Regional anesthesia can be success-fully used, with nitroglycerin available for uterine relaxation if needed.

Regional analgesia during labor and vaginal delivery has become the preferred technique of pain relief in selected high-risk patients because it prevents obtundation of the mother and depression of the fetus and reduces many of the potential adverse physiologic effects of labor, such as increased oxygen consumption and hemodynamic alterations. For cesarean section delivery, regional anesthesia has emerged as a safe and effective technique in high-risk parturients, partly because of the added ability to provide prolonged postoperative analgesia.

Approximately 1. Apart from trauma, the most common emergencies are abdominal, intracranial aneu-rysms, cardiac valvular disease, and pheochromocytoma. When the necessity for surgery arises, anesthetic considerations are related to the alterations in maternal physiologic condition with advancing pregnancy, the teratogenicity of anesthetic drugs, the indirect effects of anesthesia on uteroplacental blood flow, and the potential for abortion or premature delivery.

The risks must be balanced to provide the most favorable outcome for mother and child. Five major studies have attempted to relate surgery and anesthesia during human pregnancy to fetal outcome as determined by anomalies, premature labor, or intrauterine death.

Although these studies failed to correlate surgery and anesthetic exposure with congenital anomalies, all studies demonstrated an increased incidence of fetal death, particularly after operations performed in the first trimester. No particular anesthetic agent or technique was implicated. We are all individuals and there is no hard rule or absolutes about survivability as it relates to staging.

But I get so many emails about this topic that I have to alter form here and make some personal and subjective observations…. You are likely on this page because someone has told you that you are a certain stage cancer. Staging and statistics can throw a newly diagnosed patient into confusion. The first rule of thumb is that no doctor can tell you absolutely what your chances are of being cured or dying no matter what stage you are. Neither can they tell you how long you will live.

Do not inquire about these things unless your doctor tells you that death is imminent and you must get your affairs in order. Even then, do not assume he can tell you for sure. He may speak from a statistical perspective, but that may not apply to you. You may be different in many ways from the population of individuals from which those statistics are derived.

For instance, they may all be older than you, or all male, or many other possible variables. He may speak from his history of personal observations, but again, that may not apply to you, and his personal experience may not reflect accurately what is happening at another institution, in other patient populations, etc.

These three following links may be of value as you contemplate your situation as a newly diagnosed cancer patient. The first is a commentary on statistics and the value of them, or perhaps the lack of value. The second is on the importance of getting a second opinion, which everyone should get as soon as possible, and is something that any quality doctor will not object to you doing. The old adage that if all you have is a hammer, everything looks like a nail, can apply to doctors as well.

Surgeons may tend to view solutions only from a surgical perspective, radiation oncologists from a radiation perspective etc. The best of all possible worlds is some type of combined therapies, and this treatment plan is best arrived at by a TUMOR BOARD at a comprehensive cancer center, or at minimum from a group of regional doctors from different disciplines, if it can be done in a timely fashion.

Please do not accept an appointment for a second consultation with another type of doctor weeks down the road. Be your own advocate. We all tend to view doctors with admiration and wonder, and most of the time we unconditionally trust their opinions. But even the best doctors can be wrong. That being said, two opinions are certainly better than one. That is why my preference is to seek out treatment in a hospital facility that has a cancer center and staff of all the different types of doctors in one place.

Go to this link on our resources page for a list of the top 50 cancer hospitals in the US. Do not let geography, as in the facility or doctor is close to home, determine your choice. You have been diagnosed with a very serious illness.

You want to be in the best facility, with the best doctors, and the most current equipment and treatment options that you can possible get yourself into, and you have ONE chance to make the best decision possible. And lastly in this personal, and subjective opinion that I am offering you here, remember that while we all think that doctors are an incredible group of individuals, some think that they have THE answer.

Here I will leave you with a lighter thought. There is a distinct difference between God and a doctor, and that is that God knows he is not a doctor. The cancer is less than 2 centimeters in size about 1 inch , and has not spread to lymph nodes in the area lymph nodes are small almond shaped structures that are found throughout the body which produce and store infection-fighting cells.

The cancer is more than 2 centimeters in size, but less than 4 centimeters less than 2 inches , and has not spread to lymph nodes in the area. Either of the following may be true: The cancer is more than 4 centimeters in size. The cancer is any size but has spread to only one lymph node on the same side of the neck as the cancer.

The lymph node that contains cancer measures no more than 3 centimeters just over one inch. Any of the following may be true: The cancer has spread to tissues around the lip and oral cavity. The lymph nodes in the area may or may not contain cancer. The cancer is any size and has spread to more than one lymph node on the same side of the neck as the cancer, to lymph nodes on one or both sides of the neck, or to any lymph node that measures more than 6 centimeters over 2 inches.

The cancer has spread to other parts of the body.