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Antiseizure effects result from blockade of voltage-sensitive sodium channels in neuronal membranes cheap 60 mg orlistat weight loss 10000 steps, an action that stabilizes hyperexcitable neurons and thereby suppresses seizure spread purchase orlistat cheap weight loss 6 months post gastric sleeve surgery. Pharmacokinetics Oxcarbazepine is well absorbed both in the presence and absence of food cheap 60mg orlistat otc weight loss pills diabetics can take. Adverse Effects The most common adverse effects are dizziness buy orlistat 120 mg with visa weight loss meal plans, drowsiness, double vision, nystagmus, headache, nausea, vomiting, and ataxia. Patients should avoid driving and other hazardous activities, unless the degree of drowsiness is low. Clinically significant hyponatremia (sodium concentration below 125 mmol/L) develops in 2. If oxcarbazepine is combined with other drugs that can decrease sodium levels (especially diuretics), monitoring of sodium levels may be needed. There is 30% cross sensitivity among patients with hypersensitivity to carbamazepine. Accordingly, patients with a history of severe reactions to either drug should probably not use the other. Oxcarbazepine has not caused the severe hematologic abnormalities seen with carbamazepine. Oxcarbazepine has been associated with serious multiorgan hypersensitivity reactions. Although manifestations vary, patients typically present with fever and rash, associated with one or more of the following: lymphadenopathy, hematologic abnormalities, pruritus, hepatitis, nephritis, hepatorenal syndrome, oliguria, arthralgia, or asthenia. Drug Interactions Oxcarbazepine induces some drug-metabolizing enzymes and inhibits others. However, it does induce enzymes that metabolize oral contraceptives and can thereby render them less effective. Oxcarbazepine inhibits the enzymes that metabolize phenytoin and can thereby raise phenytoin levels. As noted, oxcarbazepine should be used with caution in patients taking diuretics and other drugs that can lower sodium levels. Lamotrigine Therapeutic Uses Lamotrigine [Lamictal] has a broad spectrum of antiseizure activity. Mechanism of Action Benefits derive mainly from blocking sodium channels and partly from blocking calcium channels. Pharmacokinetics Administration is oral, and absorption is nearly complete, both in the presence and absence of food. Drug Interactions The half-life is dramatically affected by drugs that induce or inhibit hepatic drug-metabolizing enzymes. Estrogens can lower lamotrigine levels, whereas lamotrigine may lower progestin levels. This can create unique concerns for the provider caring for a woman of childbearing age who wants to take oral contraceptives. Adverse Effects Common side effects include dizziness, diplopia (double vision), blurred vision, nausea, vomiting, and headache. Very rarely, patients experience aseptic meningitis (inflammation of the meninges in the absence of bacterial infection). Patients who develop symptoms of meningitis—headache, fever, stiff neck, nausea, vomiting, rash, sensitivity to light—should undergo immediate evaluation to determine the cause. If no clear cause other than lamotrigine is identified, discontinuation of lamotrigine should be considered. Screen patients for suicidality before starting treatment, and monitor for suicidality during the treatment course. Gabapentin Therapeutic Uses Gabapentin [Neurontin] has a broad spectrum of antiseizure activity. Interestingly, more than 80% of prescriptions are written for off-label uses, including relief of neuropathic pain (other than postherpetic neuralgia), prophylaxis of migraine, treatment of fibromyalgia, and relief of postmenopausal hot flashes. Two forms of gabapentin are not currently indicated for management of epilepsy and, therefore, should not be confused with the form of gabapentin known as Neurontin. Owing to differences in pharmacokinetics, these forms of gabapentin are not interchangeable with each other or with Neurontin. Pharmacokinetics Gabapentin is rapidly absorbed after oral dosing and reaches peak plasma levels in 2 to 3 hours. However, as the dosage gets larger, the percentage absorbed gets smaller because, at high doses, the intestinal transport system for uptake of the drug becomes saturated. The most common side effects are somnolence, dizziness, ataxia, fatigue, nystagmus, and peripheral edema. Patients should avoid driving and other hazardous activities until they are confident they are not impaired. Pregabalin has very few interactions with other drugs, but adverse effects are common, especially dizziness and sleepiness. In contrast to most other antiseizure agents, pregabalin is regulated under the Controlled Substances Act. Therapeutic Uses Pregabalin has four approved indications: neuropathic pain associated with diabetic neuropathy, postherpetic neuralgia, adjunctive therapy of partial seizures, and fibromyalgia. Mechanism of Action Although the precise mechanism of action has not been established, we do know that pregabalin can bind with calcium channels on nerve terminals and can thereby inhibit calcium influx, which in turn can inhibit release of several neurotransmitters, including glutamate, norepinephrine, and substance P. Reduced transmitter release may underlie seizure control and relief of neuropathic pain. Pregabalin does not bind with plasma proteins but does cross the blood-brain and placental barriers. The most common are dizziness and somnolence, which often persist as long as the drug is being taken. Blurred vision may develop during early therapy but resolves with continued drug use. About 8% of patients experience significant weight gain (7% or more of body weight in just a few months). Other adverse effects include difficulty thinking, headache, peripheral edema, and dry mouth. Postmarketing reports indicate a risk for hypersensitivity reactions, including life-threatening angioedema, characterized by swelling of the face, tongue, lip, gums, throat, and larynx. Patients should discontinue pregabalin immediately at the first sign of angioedema or any other hypersensitivity reaction (blisters, hives, rash, dyspnea, wheezing). Nonetheless, patients should be instructed to report signs of muscle injury (pain, tenderness, weakness). If rhabdomyolysis is diagnosed, or even suspected, pregabalin should be withdrawn. Abuse Potential and Physical Dependence In clinical trials, 4% to 12% of patients reported euphoria as a side effect.

Drug Interactions Anticholinergic Drugs Drugs with anticholinergic properties will intensify anticholinergic responses to neuroleptics buy orlistat amex weight loss pills you can buy at walmart. Patients should be advised to avoid all drugs with anticholinergic actions order orlistat 120 mg otc weight loss quotes tumblr, including antihistamines and certain over-the-counter sleep aids discount orlistat 120mg mastercard weight loss near me. These interactions occur because levodopa and neuroleptics have opposing effects on receptors for dopamine: levodopa activates dopamine receptors order orlistat 120mg line weight loss jewelry, whereas neuroleptics cause receptor blockade. Toxicity First-generation antipsychotics are very safe; death by overdose is extremely rare. Emetics cannot be used because their effects would be blocked by the antiemetic action of the neuroleptic. Because the high-potency agents produce fewer side effects than the low- potency agents, high-potency agents are used more often. Because they cause fewer side effects, high-potency agents are generally preferred for initial therapy. Note that the incidence of these reactions is opposite to that seen with the low-potency agents. Neuroendocrine effects—galactorrhea, gynecomastia, menstrual irregularities—are seen occasionally. Fluphenazine is a high-potency agent indicated for schizophrenia and other psychotic disorders. Effects seen occasionally include sedation, orthostatic hypotension, anticholinergic effects, gynecomastia, galactorrhea, and menstrual irregularities. Trifluoperazine is a high-potency agent used for schizophrenia and other psychotic disorders. The most common adverse effects are early extrapyramidal reactions (acute dystonia, parkinsonism, akathisia). The most common adverse effects are early extrapyramidal reactions (acute dystonia, parkinsonism, akathisia) and anticholinergic effects. Medium-Potency Agents Loxapine Loxapine [Loxitane, Adasuve] is a medium-potency agent indicated only for schizophrenia. Adasuve, approved in December 2012, is used for acute treatment of agitation associated with schizophrenia. Perphenazine Perphenazine is a medium-potency agent used for schizophrenia and other psychotic disorders. Low-Potency Agents Chlorpromazine Chlorpromazine, formerly available as Thorazine, was the first modern antipsychotic medication. Additional psychiatric indications are schizoaffective disorder and the manic phase of bipolar disorder. Other uses include suppression of emesis, relief of intractable hiccups, and control of severe behavior problems in children. After oral administration, the drug is well absorbed but undergoes extensive first-pass metabolism. The most common adverse effects are sedation, orthostatic hypotension, and anticholinergic effects (dry mouth, blurred vision, urinary retention, photophobia, constipation, tachycardia). Neuroendocrine effects (galactorrhea, gynecomastia, menstrual irregularities) are seen on occasion. Photosensitivity reactions are possible, and patients should be advised to minimize unprotected exposure to sunlight. Because chlorpromazine is a low-potency neuroleptic, the risk for early extrapyramidal reactions (dystonia, akathisia, parkinsonism) is relatively low. Accordingly, patients with seizure disorders should be especially diligent about taking antiseizure medication. Because of this danger, the drug should be reserved for treating schizophrenia in patients who have not responded to safer agents. The most common adverse effects are sedation, orthostatic hypotension, anticholinergic effects, weight gain, and inhibition of ejaculation. This drug is our most effective agent for schizophrenia, the only indication it has. B l a c k B o x Wa r n i n g : A g r a n u l o c y t o s i s Clozapine can cause life-threatening agranulocytosis. Its use should be reserved for patients who have not responded to safer alternatives. In addition to blocking receptors for dopamine and serotonin, clozapine blocks receptors for norepinephrine (alpha ), histamine,1 and acetylcholine. Therapeutic Use Schizophrenia Clozapine is approved for relieving general symptoms of schizophrenia and for reducing suicidal behavior in patients with schizophrenia or schizoaffective disorder who are at chronic suicide risk. The drug is highly effective and often works when all other antipsychotics have failed. Adverse Effects and Interactions Common adverse effects include sedation and weight gain (from blocking H1 receptors); orthostatic hypotension (from blocking alpha-adrenergic receptors); and dry mouth, blurred vision, urinary retention, constipation, and tachycardia (from blocking muscarinic cholinergic receptors). Neuroendocrine effects (galactorrhea, gynecomastia, amenorrhea) and interference with sexual function are minimal. Agranulocytosis typically occurs during the first 6 months of treatment, and the onset is usually gradual. Additional testing may be completed when considering the possibility of neutropenia, when adding other antipsychotics, or when clinically indicated. When subsequent daily monitoring indicates that counts have risen above these values, clozapine can be resumed. Patients should be informed about the risk for agranulocytosis and told that clozapine will not be dispensed if the blood tests have not been done. Also, patients should be informed about early signs of infection (fever, sore throat, fatigue, mucous membrane ulceration) and instructed to report these immediately. Weight gain is the metabolic effect of greatest concern because it seems to underlie development of diabetes and dyslipidemia. Body mass index should be measured at baseline, at every visit for 6 months, and every 3 months thereafter. In addition, waist circumference should be measured at baseline and annually thereafter. If significant weight gain occurs, it can be managed with a combination of lifestyle measures and metformin, an oral drug used for diabetes. In one study, metformin was more effective than lifestyle measures, and the combination of metformin plus lifestyle measures was more effective than either intervention alone. Antipsychotic drugs promote weight gain through blockade of H receptors in the brain; they also1 cause decrease in body temperature, which decreases energy expenditure. Patients taking these drugs have developed typical diabetes symptoms, including hyperglycemia, polyuria, polydipsia, polyphagia, and dehydration. In extreme cases, hyperglycemia has led to ketoacidosis, hyperosmolar coma, and even death.

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This increased respiratory drive is due to restriction imposed on the lungs by the diaphragm elevation cheap 120mg orlistat mastercard weight loss pills venom hyperdrive 30. To understand the most common causes of respiratory disorders purchase orlistat 60 mg on-line weight loss chart, related to an acid base imbalance buy orlistat us weight loss pills 2015. Respiratory alkalosis often develops in pa­ tients with end-stage liver disease orlistat 60 mg amex weight loss yoga dvd, and the partial metabolic acidosis compensation (decreased bicarbonate level) speaks for a chronic respiratory alkalosis. One speculatedmechanism is that dimin­ ished hepatic steroid metabolism leads to elevated serum progesterone levels, which stimulate respiratory drive. This correlation exists, since the respiratory and metabolic param­ eters compensate for changes in the other. Treatment of respiratory acidosis should focus on addressing the underlying disorder. In patients with acute respiratory acidosis and hypoxemia, supplemental 0 may be administered careflly, keeping2 the 0 sat around 90% to avoid further hypercapnia. Aerosolized bronchodilators2 should be delivered under controlled Fro2 or compressed ambient air (Fro2 21%). Laboratory studies show serum sodium 140 mEq/L; potassium 5 mEq/L; chloride 100 mEq/L; and serum bicar­ bonate of 30 mEq/L. Respiratory acido­ sis with appropriate compensation (chronic respiratory acidosis) • What is the anion gap? Commoncauses of respiratory alkalosis can be sorted by condi­ tions involving the pulmonary vasculature (eg, pulmonary hypertension and venous thromboembolism), pulmonary parenchyma (eg, pulmonary fibrosis, heart failure, and pneumonia), pulmonary airways (asthma) and conditions afecting ventilatory control (eg, anxiety, aspirin toxicity, sepsis, hypoxia, and pregnancy). The expect­ ed compensatory responses for acute and chronic respiratory alkalosis are shown in Table 40-1. Example 2: A 27-year-old woman presents with a 1-day history of severe anxiety and hysteria. She is being evaluated because of weakness and dizziness and an onset of paresthesias. She had a new onset of seizures that lasted 1 minute in which she had an episode of emesis. Laboratory studies show serum sodium, 140 mEq/L; serum potassium, 5 mEq/L; serum chloride, 110 mEq/L, and serum bicarbonate of 21 mEq/L. Patients with restrictive lung diseases can only increase minute ventilation by increasing the respiratory rate. He is lethargic and weak, in moderate respiratory distress, and oriented only to place and person. Which of the fo llowing acid-base conditions is most likely present in this patient? In a patient with a diagnosis of pulmonary emboli and a chronically high respiratory rate for 5 days, the presence of a chronic respiratory alkalosis is expected. A mixed disorder should be raised in a patient whose pH is above normal in the presence of a metabolic acidosis. To confirm the suspicion of a mixed disorder, Winter formula can be used to estimate the expected Pco2: Expected Pco2 = 1. The most likely cause of a mixed anion gap metabolic acidosis and respiratory alkalosis in this patient is salicylate toxicity. This anion gap metabolic acidosis is most likely due to septic shock-associated lactic acidosis. Winter formula can be used to estimate the expected Pco for the degree of acidosis: Expected Pco2 2 = 1. The examination reveals that the patient has the same right extremity weakness as before, no new fo cal neurological fndings. Recheck serum electrolytes every 2 to 4 hours, and careflly monitor mental status and neuro­ logical examination. To learn to identif the patients "at-risk" for the development of fuid/electro­ lyte abnormalities. To learn the detrimental effects of fluid and electrolyte abnormalities and replacement strategies. However, laboratory test­ ing reveals an electrolyte abnormality, namely hyponatremia, which may explain the newly altered mental status. It usually occurs between the 2nd and lOth post-bleed day, closely paralleling the period of cerebral vasospasm. The diagnosis and management of other fluid and electrolyte abnormalities is paramount. Hyponatremia is usually asymptomatic unless the absolute level is <120 mmol/L or the change in sodium concentration is very rapid (within hours). Osmollity is the osmotic activity per volume ofwater and is expressed in mOsm/kg H20. As such, the plasma osmolality can often be considered equivalent to the plasma tonicity, also known as the efective plasma osmolality. Hyponatremia, which manifests as vague constitutional or mental status changes, can be found in up to 15% to 30% of hospitalized patients. Hyponatremia has the potential to cause substantial morbidity and mortality, and has been identified as an independent risk factorfor mortality in hospitalized patients. Moreover, overly rapid correction of chronic hyponatremia can cause severe neurological deficits and death. Sodium homeostasis: Abnormalities of plasma sodium concentration usually reflect an abnormality in total body water rather than a problem with sodium bal­ ance. To tal body water and its composition are tightly regulated by both osmotic and nonosmotic processes. Changes in plasma osmolality are monitored by the host by changes in the size of specialized neurons in the hypothalamus, called osmo­ receptors. Arterial stretch baroreceptors are located in the carotid sinus, aortic arch, cardiac atria, and pulmonary venous system. During periods of low blood volume or blood pressure, baroreceptors in the cardiac atria stimulate the adrenal release of aldosterone, which contributes to sodium and water reabsorption via the proximal renal tubule. Hyponatremia usually is a result of dysregulation of the tightly regulated process described earlier. As such, persons at risk of developing hyponatremia include those patients who are likely to have disrupted control over their water homeostasis. Detrimental effects of fluid and electrolyte abnormalities and replacement strategies: The detrimental efects of fluid and electrolyte imbalance in the inten­ sive care unit can evolve as the result of pathologic states or iatrogenically. However, symptoms may also arise secondary to very rapid changes in the serum sodium concentration. Acute hyponatremia is classified as occurring within 48 hours, whereas chronic hyponatremia takes >48 hours to develop. Initial symptoms associated with hyponatremia can be mild, including headache, nausea and vom­ iting, muscle cramps, aches, or generalized restlessness.

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Avoid placing the suture too caudally orlistat 120mg on-line weight loss zanesville ohio, as tions include a widening of the middle vault or blunting of the this may pinch the valve closed and defeat the purpose of the supra-alar creases cheap orlistat 120mg with amex weight loss 4 doctors select nutraceuticals. After graft placement order orlistat weight loss pills to lose belly fat, the dorsal aspect may be aesthetically acceptable but should be discussed with the sharply trimmed to shave off any contour irregularities or graft patient purchase orlistat line weight loss 9 weeks. On occasion, a thin fascia or perichondrium can be draped over the grafts/middle vault to ensure a smooth topog- raphy over the long-term. Medialization of the upper lateral cartilages may be cartilages but tend not to impact the angle of the valve. Patients idiopathic in origin but frequently follows a reduction rhino- with vertically oriented upper lateral cartilages may benefit plasty where the middle vault becomes destabilized and pro- from the addition of a flaring suture to reorient the upper lat- gressive soft tissue contracture leads to a pinched internal eral cartilage and directly increase the valve angle. A hump reduction involving the dorsal septum may com- nation of the flaring suture with a spreader graft has been pletely disarticulate the upper lateral cartilages off the septum, shown to lead to a statistically greater improvement in cross- 403 Revision Rhinoplasty Fig. The graft should extend from the nasal bones cephalically, just past the upper lateral cartilages caudally. The additional bulk through the caudal/lateral aspect of the upper lateral cartilage may be conspicuous if a preexisting deficiency does not exist, in a horizontal mattress fashion. The ideal location is usually creating a pollybeak deformity or excessive supratip width. On tucked under the scroll of the lateral crus, which may need to occasion, particularly with primary cases, one may need to be retracted inferiorly. Placing a cotton-tip applicator in the shave the existing dorsal septum to seat the butterfly graft in a internal valve will greatly help expose the correct area of the slight depression. The suture is draped over the nasal dor- cephalic margin of the butterfly graft to maintain a smooth sum and passed through the contralateral upper lateral carti- nasal dorsum. A full L-strut with costal cartilage (rib graft) is dorsal septum and upper lateral cartilages are weak and defi- needed to pull the nose outward and reproject the internal cient (e. This is distinct from an aesthetic dorsal vested and shaped to span over the dorsum at the internal nasal augmentation, where one might consider crushed cartilage valve. The inherent concavity makes ear cartilage an ideal graft over the dorsum to improve the profile. This cartilage reinforcement serves to augment the need structural integrity to pull the intranasal mucosa outward. The lateral aspects It is secured superiorly on the nasal bones and inferiorly at the can be suture secured to the upper lateral cartilages, thus pull- anterior nasal spine. The upper lateral cartilages can be suture ing them out in a similar way to the flaring suture. The caudal secured to the rib graft, further supporting the internal nasal end of the graft can be tucked under the cephalic border of the valve. The vestibular mucosa is carefully dissected off the row the bony nasal vault or to close an open roof deformity lateral crura to make a pocket. The osteotome is initiated 3 to 4mm above the base of the pyriform aperture and adjacent to the Fig. This will preserve the lateral position of caudal end of the upper lateral cartilages and the cephalic end of the the inferior turbinate. A small triangle of bone is preserved at the lateral crura to add structural support and flare the upper lateral pyriform aperture to maintain the airway (asterisk). In this case, low osteotomies should be performed in the high-low-high techni- osteotomies are needed and outfracturing of the bones is stabi- que, beginning 3 to 4 mm above the base of the pyriform aper- lized with nasal packing. These maneuvers have been shown to ture and anterior/superior to the head of the inferior turbinate increase the cross-sectional area with proper patient selec- 3 tion. If medialization of the inferior turbinate is noted after completion of the osteotomy technique, the inferior turbi- drilled open through the sublabial route. These maneuvers are of the nasal obstruction is excessive narrowing of the bony pyri- typically last-ditch efforts in functional rhinoplasty. The left flap is designed as a crescentic island flap and is rotated medially to lateralize the alar base. An alar base flap to correct nostril and vestibular stenosis and alar base malposition in rhinoplasty. When complex, tioning of the alar lobules (Weir excision) is often used in cos- traditional septoplasties, not to mention submucous resection metic rhinoplasty to reduce nostril size and to narrow the alar and endoscopic techniques, will invariably fail. This may lead to vestibular stenosis, alar base malposition, 18 sary to explant the deformed portions, reorient and straighten, and nasal obstruction. The autogenous graft should cutaneous and musculocutaneous perforators has been be firmly suture secured to the remaining septum and anterior described independently by Constantian and Meyer to address nasal spine. Careful quilting sutures through the mucoperichon- obstruction that accompanies vestibular stenosis and alar base drial flaps will lend additional support. The flap is elevated based on sub- Dysfunction of the intervalve area is the most common etiology cutaneous and musculocutaneous perforators and on branches of iatrogenic lateral nasal wall collapse, owing to overresection from the angular artery. The flap is then inserted into the nos- of the lateral crura during cephalic trim or excessive narrowing tril sill and floor by reopening the nostril at the site of the pre- of the nasal tip with sutures that pull the lateral crura inward. In patients with prior alar base incisions, the blood 10mm, and avoid resection in patients with vertically oriented supply to the nasal tip may be predominately through the col- lateral crura (parenthesis deformity). Opening the nose in this circumstance may binding sutures, one must recognize any evidence of crural compromise blood supply to the tip and result in tip necrosis. Poorly placed marginal and rim incisions may lead to wound Surgical correction of intervalve collapse is primarily contraction and cicatricial stenosis after rhinoplasty. Mild achieved through lateral wall batten grafts that add support to deformities may be addressed with the use of Z-plasties to the nasal sidewall, resist collapse on inspiration, and pull the lengthen the contraction and decrease the stenotic segment. Although these bat- When the stenosis is more involved, repair often requires the ten grafts may result in added fullness to the supra-alar region use of composite grafts harvested from the auricle. These grafts in a minority of patients, a study by Toriumi et al revealed that will provide the internal lining and cartilaginous support to patients were willing to accept this in light of the relief in nasal resist contraction and reformation of the cicatricial stenosis. When this corresponds with the nasal ala (uncom- tion, rerotation, and suspension of the nasal tip to correct the mon), it is referred to as an alar batten graft. One way to improve tip pro- the nasal sidewall or intervalve area, the graft is referred to as a jection is to disarticulate the medial crura and resecure them to sidewall batten graft. Conchal cartilage serves as an excellent the caudal border of the septal cartilage, increasing projection. The graft is placed in a soft tissue pocket extending to the bony pyriform aperture. The graft is placed at the epicenter of collapse, at the intervalve area (a, left) or at the external valve (a, right). Conchal cartilage placed at the (b) intervalve area and at the (c) external valve. The graft is placed and secured with a rapidly absorb- carved into a crescentic shape with beveled edges and a ing suture, as in the open approach. It Failure to recognize the parenthesis deformity in primary rhi- is critical for the graft to be long enough to overlap the existing noplasty may result in dysfunction at the intervalve area. The lateral crural cartilage and extend laterally to the bony pyriform parenthesis deformity describes cephalically positioned, verti- aperture. Treatment consists of transposition When placed through the open approach, a soft tissue pocket of the malformed lateral crura into a more physiologic position. The graft is secured with a obstruction when reducing tip bulbosity—especially when rapidly absorbing suture placed through the nasal mucosa, pull- dome-binding sutures are placed.

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C Continuous electronic fetal monitoring should be advised for women with signifcant meconium stained liquor discount orlistat online weight loss breakfast ideas, which is either dark green or black 120 mg orlistat mastercard weight loss pills xls, thick buy orlistat 120mg without a prescription weight loss 90, tenacious containing lumps of meconium cheap orlistat 60mg line weight loss inspirational quotes. If there are no contraindications, and continuous monitoring is not feasible due to loss of contact with external monitors, fetal scalp electrode monitoring is the method of choice. C When there is a delay in the established frst stage of labour, the use of oxytocin should be considered and advice should be sought from an obstetrician. Women should be informed that oxytocin use afer spontaneous rupture of membranes will bring forward her time of birth, but will not infuence the mode of delivery or other outcomes. I Tere is a delay in the established frst stage of labour where there is only 1 cm dilatation in 4 hours in a parous woman. A Tere is a good progress of labour during the established frst stage of labour and during the second stage with no evidence of fetal compromise, hence no intervention is necessary and one should await the vaginal delivery to take place. The last category requires intermittent auscultation unless the clinical situation changes during labour. It is important to explain the risks and benefts to women who require continuous intrapartum fetal monitoring. A digital vaginal exam should be avoided in the absence of contractions to minimize the risk of infection (chorioamnionitis). However, she should be warned about the signs of infection and advised to take temperature every 4 hourly. If she feels unwell and has raised temperature or reduced fetal movements she should seek immediate medical advice. If she does not go into labour within 24 hours, induction of labour is recommended due to increased risk of infection to both the fetus (the risk of serious neonatal infection is about 1%) and the mother. Women with prolonged rupture of the membranes (24–36 hours) may need prophylactic antibiotics during labour until delivery, even if there is no clinical evidence of infection. It is commonly undertaken when labour fails to start spontaneously by 10 days past the due date. An ultrasound scan in early pregnancy (before 20 weeks) can help to determine the due date more accurately and reduces the chances of unnecessary induction. It has been shown to increase the chances of labour starting spontaneously within the next 48 hours and can reduce the need for other methods of induction of labour. Tere is no evidence to suggest that labour induced with prostaglandins is any more painful than labour that has started spontaneously. The frst step is rupture of membranes, which is generally artifcial rupture of membranes. This is an obstetric emergency and the delivery of the baby should be performed immediately. It can be used for induction of labour in women with spontaneous rupture of membranes, augmentation of labour in women with poor progress of labour and active management of third stage of labour to prevent postpartum haemorrhage. The indications for β agonist usage include: (a) allowing time while administering steroids to mother to promote fetal lung maturity; or (b) if the fetus requires intrauterine transfer to another hospital. Further use of oxytocin may not be efective as prolonged administration of oxytocin down-regulates its own receptor. Prolonged use of oxytocin also causes vasodilatation, hypotension, tachycardia and hyponatraemia. This can cause sudden collapse in an already compromised woman and may lead to death. On the other hand it can also cause water retention due to some of its antidiuretic action. Tey promote contraction of the uterine muscle and therefore reduce postpartum blood loss. The other uses of oxytocin include management of excessive bleeding afer miscarriage or abortion. The side efects of oxytocin include nausea, vomiting, cramping, light-headedness, water retention and hyponatraemia. It allows assessment of liquor colour and helps to rule out cord prolapse or presentation. Where there is a persuasive history of rupture of membranes but no liquor seen even on coughing, then a speculum examination can be repeated afer 1 hour of the patient lying supine, which allows liquor to pool in the vagina. In this situation delivery should be expedited (within 30 minutes of diagnosis and decision). One should also take caution not to perform a difficult instrumental delivery because of the increased risk of intracranial bleeding. Afer delivery, paired cord blood sampling for pH and base excess should be collected. The risk of intrauterine death, meconium stained liquor and oligohydramnios increases with postmaturity. Acceleration: should be present (defned as increase of the fetal heart beat of more than 15 beats above baseline and lasting for 15 seconds) 4. Terefore, one should either deliver the fetus within 30 minutes if indicated or perform fetal blood sampling to check if the fetus is compromised. This is a clinical decision and would depend on the overall clinical circumstances. The time taken to take a fetal blood sample needs to be considered when planning repeat samples. One should ensure that the woman has a large bore cannula and group and save if she is bleeding vaginally. Informed consent should be taken before the procedure and the cavity should be checked to ensure it is empty afer the procedure. She would also need prophylactic intravenous antibiotics at the time of induction to decrease the risk of uterine infection. Afer the procedure, the uterus should be kept contracted by using syntocinon 40 units infusion as well as by insertion of rectal misoprostol (600–1000 µg). The other risk factors for shoulder dystocia include maternal obesity, diabetes (increases the risk of shoulder dystocia by more than 70%), fetal macrosomia, previous shoulder dystocia (12% recurrence in future pregnancies), prolonged labour (labour progresses normally in 70% of women) and difcult instrumental delivery. Shoulder dystocia is defned as failure to deliver the shoulders afer the head has been delivered. Early induction of labour in women with fetal macrosomia does not reduce either shoulder dystocia or the caesarean section rate. Elective caesarean section is not recommended for women with fetal macrosomia on scan as this has not been shown to decrease operative delivery or shoulder dystocia or birth trauma. It is reasonable to do a planned caesarean section in diabetic women with birth weight more than 4500 gm. Episiotomy scar or scar from perineal tear both might cause dyspareunia requiring refashioning of the perineum. Routine use of oxytocin in the second stage reduces the risk of postpartum haemorrhage. Prophylactic oxytocics should be ofered routinely to all women in the third stage of labour to reduce the risk of postpartum haemorrhage.

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