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First_Aid_Step2. More common in males than in females, except for meningiomas. Symptoms depend on tumor type and location (see Table 2.10-10), local growth and resulting mass effect, cerebral edema, or elevated ICP 2° to ventricular obstruction. Although headaches are often thought of as the main presenting symptom, only 31% of patients present with headache at diagnosis and only 8% have headache as the sole presenting feature. Seizures or slowly progressive focal motor deficits are the most common presenting features. When ↑ ICP is the presenting feature, symptoms include headache, nausea/vomiting, and diplopia (false localizing CN VI palsies). However, in the era of neuroimaging, it is relatively rare for patients to present with ↑ ICP.


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First_Aid_Step2. Hemispheric tumors often produce visual field abnormalities and neuropsychiatric symptoms, including personality changes, lethargy, syncope, cognitive decline, aphasia, apraxia, and depression. Parasellar lesions usually present with visual loss and/or diplopia. Posterior fossa lesions tend to present with gait ataxia or cranial nerve deficits and/or ↑ ICP from obstructive hydrocephalus. Metastases that tend to present with intracranial hemorrhage include renal cell carcinoma, thyroid cancer, choriocarcinoma, and melanoma. ■Contrast CT and MRI with and without gadolinium to localize and determine the extent of the lesion. Gadolinium-enhanced MRI is generally better for visualizing soft tissue tumors and vascularity, but CT is better for TABLE 2.10-10. Common 1° Neoplasms


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First_Aid_Step2. Astrocytoma Arises in brain parenchyma. Low-grade astrocytomas are relatively uncommon. Presents with seizures, focal defcits, or headache. Has a protracted course. Has a better prognosis than glioblastoma multiforme (see below). Resection if possible; radiation. Glioblastoma multiforme (grade IV astrocytoma) High mitotic activity and either endothelial proliferation or necrosis in tumor, leading to ring-enhancing lesions on MRI. There is a major difference between grade III and grade IV. The most common 1° brain tumor. Presents with headache and ↑ seizures, focal def cits, or headache. Progresses rapidly and has a poor prognosis (< 1 year from the time of prognosis). Surgical removal/resection. Radiation and chemotherapy have variable results. Meningioma Originates from the dura mater or arachnoid. Presentation depends on location; often related to cranial neuropathy or is an incidental f nding. Good prognosis. Incidence ↑ with age. Imaging may reveal dural tail. Surgical resection;


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First_Aid_Step2. arachnoid. Presentation depends on location; often related to cranial neuropathy or is an incidental f nding. Good prognosis. Incidence ↑ with age. Imaging may reveal dural tail. Surgical resection; radiation for unresectable tumors. Acoustic neuroma (schwannoma) Derived from Schwann cells. Presents with ipsilateral tinnitus, hearing loss, vertigo, and late signs of CN V–VII or brain stem compression. Surgical removal. A primitive neuroectodermal tumor. Arises from the fourth ventricle and causes ↑ ICP. Common in children. Highly malignant; may seed the subarachnoid space. May cause obstructive hydrocephalus. Surgical resection coupled with radiation and chemotherapy. May arise from the ependyma of a ventricle (commonly the fourth) or the spinal cord. Common in children; low grade. May cause obstructive hydrocephalus. Surgical resection; radiation. Medulloblastoma Ependymoma evaluating skull base lesions and for emergencies (e.g., obstructive hydrocephalus) when an MRI cannot be


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First_Aid_Step2. cause obstructive hydrocephalus. Surgical resection; radiation. Medulloblastoma Ependymoma evaluating skull base lesions and for emergencies (e.g., obstructive hydrocephalus) when an MRI cannot be rapidly acquired.


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First_Aid_Step2. ■Histologic diagnosis via CT-guided biopsy or surgical tumor debulking/ removal. Resection (if possible), radiation, and chemotherapy. Therapy is highly dependent on tumor type, histology, progression, and site (see Table 2.10-10). Corticosteroids can be used to ↓ vasogenic edema and ↓ ICP. Management is often palliative. Seizure prophylaxis can be used in patients who have had a seizure. Symptoms of ↑ ICP: Headache that is worse in the morning or with recumbency In NF1, you— spots) NN (2 Neurof bromas) OT (OpTic glioma) FAI (Freckling, Axillary relative with NF1) NF1 and NF2 are clinically evident by ages 15 and 20, respectively. If you see infantile spasms in the setting of a hypopigmented lesion on the child’s trunk, consider tuberous sclerosis.


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First_Aid_Step2. NF1 and NF2 are clinically evident by ages 15 and 20, respectively. If you see infantile spasms in the setting of a hypopigmented lesion on the child’s trunk, consider tuberous sclerosis. The most common neurocutaneous disorder. There are two major types: neurofibromatosis 1 (NF1, or von Recklinghausen’s syndrome) and neurofibromatosis 2 (NF2). Both obey autosomal-dominant inheritance. The NF genes are located on chromosome 17 and 22, respectively, for NF1 and NF2. Diagnostic criteria for NF1 include two or more of the following: Six café au lait spots (each ≥ 5 mm in children or ≥ 15 mm in adults). Two neurofibromas of any type. Freckling in the axillary or inguinal area. Optic glioma. Two Lisch nodules (pigmented iris hamartomas). Bone abnormality (e.g., kyphoscoliosis). A f rst-degree relative with NF1. Diagnostic criteria for NF2 are as follows:


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First_Aid_Step2. Optic glioma. Two Lisch nodules (pigmented iris hamartomas). Bone abnormality (e.g., kyphoscoliosis). A f rst-degree relative with NF1. Diagnostic criteria for NF2 are as follows: Bilateral acoustic neuromas or a first-degree relative with NF2 and either unilateral acoustic neuromas or two of any of the following: neurofibromas, meningiomas, gliomas, or schwannoma. Other features include seizures, skin nodules, and café au lait spots. MRI of the brain, brain stem, and spine with gadolinium. Obtain a complete dermatologic exam, ophthalmologic exam, and family history. Auditory testing is recommended. There is no cure; treatment is symptomatic (e.g., surgery for kyphoscoliosis or debulking of tumors). Acoustic neuromas and optic gliomas can be treated with surgery or radio-surgery. Meningiomas may be resected. Affects many organ systems, including the CNS, skin, heart, retina, and kidneys. Obeys autosomal-dominant inheritance.


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First_Aid_Step2. Affects many organ systems, including the CNS, skin, heart, retina, and kidneys. Obeys autosomal-dominant inheritance. Presents with convulsive seizures (infantile spasms in infants),“ash-leaf” hypopigmented lesions on the trunk and extremities, and mental retardation (↑ likelihood with early age of onset). Other skin manifestations include sebaceous adenomas (small red nodules on the nose and cheeks in the shape of a butterﬂy) and a shagreen patch (a rough papule in the lumbosacral region with an orange-peel consistency). Two retinal lesions are recognized: (1) mulberry tumors, which arise from the nerve head; and (2) phakomas, which are round, ﬂat, gray lesions located peripherally in the retina. Symptoms are 2° to small benign tumors that grow on the face, eyes, brain, kidney, and other organs. Mental retardation and CHF from cardiac rhabdomyoma may also be seen. Renal involvement may include hamartomas, angiomyolipomas, or, rarely, renal cell carcinoma.


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First_Aid_Step2. Mental retardation and CHF from cardiac rhabdomyoma may also be seen. Renal involvement may include hamartomas, angiomyolipomas, or, rarely, renal cell carcinoma. Diagnosis is usually clinical. Skin lesions are enhanced by a Wood’s UV lamp. Imaging: Head CT: Reveals calcified tubers within the cerebrum in the periventricular area. Lesions may on rare occasion transform into malignant astrocytomas. ECG: Evaluate for rhabdomyoma of the heart, especially in the apex of the left ventricle (affects > 50% of patients). Renal ultrasound: May reveal renal hamartomas, masses, or polycystic disease. Renal CT: May show angiomyolipomas (causing cystic or fibrous pulmonary changes). CXR: May reveal pulmonary lesions or cardiomegaly 2° to rhabdomyoma. Treatment should be based on symptoms (e.g., cosmetic surgery for adenoma sebaceum).


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First_Aid_Step2. CXR: May reveal pulmonary lesions or cardiomegaly 2° to rhabdomyoma. Treatment should be based on symptoms (e.g., cosmetic surgery for adenoma sebaceum). Simple partial or complex partial seizures can be controlled with oxcarbazepine or carbamazepine; lamotrigine can be given for generalized seizures. Treat infantile spasms with ACTH or vigabatrin. Surgical intervention may be indicated in the setting of ↑ ICP or for seizures associated with an epileptogenic focus or severe developmental delay. A general term for speech and language disorders. Usually results from insults (e.g., strokes, tumors, abscesses) to the “dominant hemisphere” (the left hemisphere in > 95% of right-handed people and 60–80% of left-handed people). ■ A disorder of language production, including writing, with intact comprehension. Due to an insult to Broca’s area in the posterior inferior fron Broca’s aphasia is also known tal gyrus. Often 2° to a left superior MCA stroke. Also known as motor aphasia.


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First_Aid_Step2. Broca’s aphasia is also known tal gyrus. Often 2° to a left superior MCA stroke. Also known as motor aphasia. Hx/PE: Presents with impaired repetition, frustration with awareness of aphasia. deficits, arm and facial hemiparesis, hemisensory loss, and apraxia of the oral muscles. Speech is described as “telegraphic” and agrammatical with frequent pauses. Tx: Speech therapy (varying outcomes with intermediate prognosis). Wernicke’s Aphasia Wernicke’s aphasia is also known as f uent or receptive ■ A disorder of language comprehension with intact yet nonsensical production. Also known as sensory aphasia. aphasia. BROca’s is BROken and Wernicke’s is Wordy. Due to an insult to Wernicke’s area in the left posterior superior temporal (perisylvian) gyrus. Often 2° to left inferior/posterior MCA embolic stroke.


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First_Aid_Step2. BROca’s is BROken and Wernicke’s is Wordy. Due to an insult to Wernicke’s area in the left posterior superior temporal (perisylvian) gyrus. Often 2° to left inferior/posterior MCA embolic stroke. Hx/PE: Presents with preserved f uency of language with impaired repetition and comprehension, leading to “word salad.” Patients are unable to follow commands; make frequent use of neologisms (made-up words) and paraphasic errors (word substitutions); show lack of awareness of deficits; and exhibit right upper homonymous quadrantanopia 2° to involvement of Meyer’s loop. Tx: Treat the underlying etiology and institute speech therapy.


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First_Aid_Step2. Tx: Treat the underlying etiology and institute speech therapy. A state of unconsciousness marked by a profound suppression of responses to external and internal stimuli (i.e., a state of unarousable unresponsiveness). Lesser states of impaired arousal are known as “obtundation” or “stupor.” Coma is due to either catastrophic structural CNS injury or diffuse metabolic dysfunction. Coma indicates bilateral dysfunction of both cerebral hemispheres or the brain stem (pons or higher); when structural, coma usually results from bilateral pathology. Causes include the following: Diffuse hypoxic/ischemic encephalopathy (e.g., postcardiac arrest). Diffuse axonal injury from high-acceleration trauma (e.g., MVA). Brain herniation (e.g., cerebral mass lesion, SAH with obstructive hydrocephalus). Widespread infection (e.g., viral encephalitis or advanced bacterial meningitis). Massive brain stem hemorrhage or infarction (e.g., pontine myelinolysis).


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First_Aid_Step2. Widespread infection (e.g., viral encephalitis or advanced bacterial meningitis). Massive brain stem hemorrhage or infarction (e.g., pontine myelinolysis). Electrolyte disturbances (e.g., hypoglycemia). Exogenous toxins (e.g., opiates, benzodiazepines, EtOH, other drugs). Generalized seizure activity or postictal states. Endocrine (e.g., severe hypothyroidism) or metabolic dysfunction (e.g., thiamine deficiency). Obtain a complete medical history from witnesses, including current medications (e.g., sedatives). Conduct thorough medical and neurologic exams, including assessments of mental status, spontaneous motor activity, muscular tone, breathing pattern, funduscopy, pupillary response, eye movements (including the doll’seye maneuver if the neck has been cleared from fracture), corneal reﬂ ex, cold-water caloric testing, gag reﬂex, and motor or autonomic responses to noxious stimuli applied to limbs, trunk and face (e.g., retromandibular pressure, nasal tickle).


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First_Aid_Step2. Typically made by a combination of the history/physical and laboratory tests or neuroimaging. Check glucose, electrolytes, calcium, a renal panel, LFTs, ABG, a toxicology screen, and blood and CSF cultures. Other metabolic tests (e.g., TSH) may be performed based on the clinical index of suspicion. Obtain a head CT without contrast before other imaging to evaluate for hemorrhage or structural changes. Imaging should precede LP in light of the risk of herniation. Obtain an MRI to exclude structural changes and ischemia (e.g., brain stem). EEG may be both diagnostic and prognostic. Rule out catatonia, hysterical or conversion unresponsiveness, “locked-in” syndrome, or persistent vegetative state (PVS), all of which can be confused with true coma (see Table 2.10-11). “Locked-in” syndrome: Patients are awake and alert but can move only their eyes and eyelids. Associated with central pontine myelinolysis, brain stem stroke, and advanced ALS.


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First_Aid_Step2. “Locked-in” syndrome: Patients are awake and alert but can move only their eyes and eyelids. Associated with central pontine myelinolysis, brain stem stroke, and advanced ALS. PVS: Characterized by normal wake-sleep cycles but lack of awareness of self or the environment. The most common causes are trauma with diffuse cortical injury or hypoxic ischemic injury. Initial treatment should consist of the following measures: Stabilize the patient: Attend to ABCs. Reverse the reversible: Administer DONT—Dextrose, Oxygen, Naloxone, and Thiamine. Identify and treat the underlying cause and associated complications. Prevent further damage. Table 2.10-12 describes the neurologic symptoms commonly associated with nutritional deficiencies. Figure 2.10-8 illustrates common visual field defects and the anatomic areas with which they are associated. T AB LE 2.1 0-1 1. Differential Diagnosis of Coma


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First_Aid_Step2. Figure 2.10-8 illustrates common visual field defects and the anatomic areas with which they are associated. T AB LE 2.1 0-1 1. Differential Diagnosis of Coma Alertness Wakeful and alert with retained cognitive abilities. Wakefulness without awareness. Unconscious; no sleep-wake cycles. Unconscious; no sleep-wake cycles. Most common causes Central pontine myelinolysis, brain stem stroke, advanced ALS. Diffuse cortical injury or hypoxic ischemic injury. See above. Same as coma. Voluntary motor ability Eyes and eyelids. None. None. None. Respiratory drive Yes. Yes. Yes. None. T AB LE 2.1 0-1 2. Neurologic Syndromes Associated with Nutritional Deficiencies


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First_Aid_Step2. Thiamine (vitamin B1) Wernicke’s encephalopathy Korsakoff’s dementia The classic triad consists of encephalopathy (disorientation, inattentiveness, confusion, coma), ophthalmoplegia (nystagmus, lateral rectus palsy, conjugate gaze palsy, vertical gaze palsy), and ataxia (polyneuropathy; cerebellar and vestibular dysfunction leading to problems standing or walking). Above, plus anterograde and retrograde amnesia, horizontal nystagmus, and confabulations. Alcoholics, hyperemesis, starvation, renal dialysis, AIDS. Can be brought on or exacerbated by high-dose glucose administration. Same as above. Usually occurs in the “resolution” phase of Wernicke’s syndrome that was treated late or inadequately. Reversible almost immediately with thiamine administration. Always give thiamine before glucose. Irreversible. Cyanocobalamin (vitamin B12)a Combined system disease (CSD) or subacute combined degeneration of the posterior and lateral columns of the spinal cord (see the discussion of clinical


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First_Aid_Step2. Irreversible. Cyanocobalamin (vitamin B12)a Combined system disease (CSD) or subacute combined degeneration of the posterior and lateral columns of the spinal cord (see the discussion of clinical neuroanatomy); peripheral neuropathy. Gradual, progressive onset. Symmetric paresthesias, stocking-glove sensory neuropathy, leg stiffness, spasticity, paraplegia, bowel and bladder dysfunction, sore tongue. Dementia. Patients with pernicious anemia; strict vegetarians; status post gastric or ileal resection; ileal disease (e.g., Crohn’s); alcoholics or others with malnutrition. B12 injections or large oral doses. Folatea Folate def ciency Irritability; personality changes without the neurologic symptoms of CSD. Alcoholics; patients with pernicious anemia. Reversible if corrected early. a Associated with ↑ homocysteine and ↑ risk of vascular events.


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First_Aid_Step2. In the eye, aqueous humor is produced by the ciliary body on the iris, travels through the pupil into the anterior chamber, and is then drained via the trabecular meshwork in the angle of the anterior chamber. ■Any process that disrupts this natural ﬂ ow can ↑ intraocular pressure (IOP), damaging the optic nerve and causing visual field deficits. Glaucoma is the result of such damage to the nerve. 1. 2. 3. 4. 5. 6. Left hemianopia with macular sparing FIGURE 2.10-8. Visual field defects. Defect in visual field of Lt. eye Rt. eye 1 2 3 4 Optic chiasm Optic nerve Optic tract loop Calcarine fissure Visual cortex 1 5 3 2 Dorsal optic radiation Lt. Rt. Lateral geniculatebody ■Open-angle glaucoma is much more common in the United States than closed-angle glaucoma.


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First_Aid_Step2. Occurs when the iris dilates and pushes against the lens of the eye, disrupting ﬂow of aqueous humor into the anterior chamber. Pressure in the posterior chamber then pushes the peripheral iris forward and blocks the angle. Risk factors include family history, older age, Asian ethnicity, hyperopia, prolonged pupillary dilation (prolonged time in a dark area, stress, medications), anterior uveitis, and lens dislocation. Hx/PE: Classically presents with extreme eye pain, blurred vision, headache, nausea, and vomiting. A hard, red eye is seen (from acute closure of a narrow anterior chamber angle); the pupil is dilated and nonreactive to light. IOP is ↑. If it resolves spontaneously prior to presentation (e.g., with pupillary constriction in sunlight), ophthalmologic examination may reveal narrow angles in one or both eyes.


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First_Aid_Step2. Dx: Diagnosis is based on clinical history and examination. Those that resolve may mimic a migraine headache with blurred vision; the distinction is that the headaches and blurred vision are more likely to be triggered by darkness (due to pupillary dilation) rather than by bright lights (migraine). Tx: This is a medical emergency that can cause blindness. Treatment to ↓ IOP may include eyedrops (timolol, pilocarpine, apraclonidine) or systemic medications (oral or IV acetazolamide, IV mannitol). Laser peripheral iridotomy, which creates a hole in the peripheral iris, is curative and may be performed prophylactically. generally occurs bilaterally, ■Flow of aqueous humor through the trabecular meshwork is limited, in- creasing IOP. A diseased trabecular meshwork obstructs proper drainage of the eye, leading to a gradual ↑ in pressure and progressive vision loss. occurs unilaterally.


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First_Aid_Step2. In the United States, macular degeneration is the leading cause of permanent bilateral visual loss in the elderly. Risk factors include age > 40 years, African-American ethnicity, diabetes, and myopia. Hx/PE: Usually asymptomatic until late in the clinical course, when patients may begin to notice visual deficits. Should be suspected in patients > 35 years of age who need frequent lens changes and have mild headaches, visual disturbances, and impaired adaptation to darkness. The earliest visual defect is seen in the peripheral nasal fields. Cupping of the optic nerve head is seen on funduscopic exam. Dx: Tonometry, ophthalmoscopic visualization of the optic nerve, and visual field testing are most important. A diseased trabecular meshwork obstructs proper drainage of the eye, gradually increasing pressure and leading to progressive vision loss.


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First_Aid_Step2. Tx: Treat with topical β-blockers (timolol, betaxolol) to ↓ aqueous humor production or with pilocarpine to ↑ aqueous outﬂow. Carbonic anhydrase inhibitors may also be used. If medication fails, laser trabeculoplasty or a trabeculectomy can improve aqueous drainage. More common among Caucasians, females, smokers, and those with a family history. Presents with painless loss of central vision. Atrophic (“dry”) macular degeneration: Responsible for 80% of cases. Causes gradual vision loss. Exudative or neovascular (“wet”) macular degeneration: Much less common, but associated with more rapid and severe vision damage. Funduscopy by an ophthalmologist reveals drusen and/or pigmentary changes in patients with atrophic AMD. Hemorrhage and subretinal ﬂuid are suggestive of exudative AMD. Atrophic AMD: No treatment is currently available, although a combination of vitamins (vitamin C, vitamin E, beta-carotene, and zinc) has been found to slow disease progression.


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First_Aid_Step2. Atrophic AMD: No treatment is currently available, although a combination of vitamins (vitamin C, vitamin E, beta-carotene, and zinc) has been found to slow disease progression. An ↑ mortality rate from high doses of vitamin E and an elevated lung cancer incidence among individuals on beta-carotene supplementation may require modification of this regimen for smokers. Exudative AMD: VEGF inhibitors have been shown to improve vision (ranibizumab, bevacizumab) or slow visual loss (pegaptanib) in patients with exudative AMD. Photodynamic therapy with verteporfin, which involves use of a laser to selectively target retinal vessels, may be useful in conjunction with VEGF inhibitors. Occurs in elderly patients and is often idiopathic. Hx/PE:


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First_Aid_Step2. Occurs in elderly patients and is often idiopathic. Hx/PE: Central retinal artery occlusion: Presents with sudden, painless, unilateral blindness. The pupil reacts to a near stimulus but is sluggishly reactive to direct light. Patients present with a cherry-red spot on the fovea, retinal swelling (whitish appearance to the nerve fiber layer), and retinal arteries that may appear bloodless. Central retinal vein occlusion: Characterized by rapid, painless vision loss of variable severity. A choked, swollen optic disk with hemorrhages, venous stasis retinal hemorrhages, cotton-wool spots, and edema of the macula may be seen on funduscopic exam. Tx:


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First_Aid_Step2. Tx: Central retinal artery occlusion: Intra-arterial thrombolysis of the ophthalmic artery within eight hours of onset of symptoms may produce benefit in some patients, although evidence remains controversial. Other treatments applied but of unclear benefit include increasing IOP through drainage of the anterior chamber or IV acetazolamide. If implemented, treatments should be applied immediately before irreversible retinal infarction and permanent blindness ensue. Central retinal vein occlusion: Laser photocoagulation has variable results. Physiology of Normal Pregnancy 321 THE BASICS OF PREGNANCY 321 NORMAL PHYSIOLOGY OF PREGNANCY 321 Teratology 325 Maternal-Fetal Infections 326 Spontaneous Abortion 328 Elective Termination of Pregnancy 329 Normal Labor and Delivery 329 Medical Complications of Pregnancy 336 HYPEREMESIS GRAVIDARUM 336 DIABETES IN PREGNANCY 338 GESTATIONAL AND CHRONIC HYPERTENSION 340 PREECLAMPSIA AND ECLAMPSIA 340 ANTEPARTUM HEMORRHAGE 342


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First_Aid_Step2. Medical Complications of Pregnancy 336 HYPEREMESIS GRAVIDARUM 336 DIABETES IN PREGNANCY 338 GESTATIONAL AND CHRONIC HYPERTENSION 340 PREECLAMPSIA AND ECLAMPSIA 340 ANTEPARTUM HEMORRHAGE 342 Obstetric Complications of Pregnancy 342 ECTOPIC PREGNANCY 342 INTRAUTERINE GROWTH RESTRICTION 344 FETAL MACROSOMIA 345 POLYHYDRAMNIOS 345 OLIGOHYDRAMNIOS 345 Rh ISOIMMUNIZATION 345 GESTATIONAL TROPHOBLASTIC DISEASE 346 MULTIPLE GESTATIONS 348 Abnormal Labor and Delivery 348 SHOULDER DYSTOCIA 348 FAILURE TO PROGRESS 348 RUPTURE OF MEMBRANES 349 PRETERM LABOR 350 FETAL MALPRESENTATION 351 INDICATIONS FOR CESAREAN SECTION 351 EPISIOTOMY 353 The Basics of Pregnancy The following terms and concepts are central to an understanding of the physiologic processes of pregnancy (see also Figure 2.11-1). Gravidity: The number of times a woman has been pregnant. Parity: The number of pregnancies that led to a birth beyond 20 weeks’ gestational age or an infant weighing > 500 g.


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First_Aid_Step2. Gravidity: The number of times a woman has been pregnant. Parity: The number of pregnancies that led to a birth beyond 20 weeks’ gestational age or an infant weighing > 500 g. Developmental age (DA): The number of weeks and days since fertilization. Typically used only in research, as the exact date of fertilization is not commonly known. Gestational age (GA): The number of weeks and days measured from the frst day of the last menstrual period (LMP). GA can also be determined by: Fundal height: At 20 weeks, the uterus is at the umbilicus and grows approximately 1 cm/week. Quickening, or appreciation of fetal movement: Typically occurs at 17–18 weeks. Fetal heart tones: Can be heard at 10–12 weeks by Doppler. Ultrasound: Measures fetal crown-rump length (CRL) at 5–12 weeks and measures biparietal diameter (BPD), femur length (FL), and abdominal circumference (AC) from 13 weeks. Ultrasound measurement of GA is most reliable during the f rst trimester.


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First_Aid_Step2. Normal Physiology of Pregnancy The normal physiologic changes that occur during pregnancy are graphically illustrated according to system in Figures 2.11-2 and 2.11-3. Nägele’s rule: due date = last menstrual period + nine months + seven days. F IGU R E 2.1 1 -1. Perinatal nomenclature by date. (Reproduced, with permission, from DeCherney AH, Nathan L. Current Diagnosis & Treatment: Obstetrics & Gynecology, 10th ed. New York: McGraw-Hill, 2007: Fig. 9-1.) (Reproduced, with permission, from Gardner DG, Shoback D. Greenspan’s Basic & Clinical Endocrinology, 8th ed. New York: McGraw-Hill, 2007: Fig. 17-2A.) The goal of prenatal care is to prevent, diagnose, and treat conditions that can lead to adverse outcomes in pregnancy. Expected weight gain, nutrition, and exercise recommendations are outlined in Table 2.11-1. Get a quantitative β-hCG: To diagnose and follow ectopic pregnancy. To monitor trophoblastic disease. To screen for fetal aneuploidy.


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First_Aid_Step2. Get a quantitative β-hCG: To diagnose and follow ectopic pregnancy. To monitor trophoblastic disease. To screen for fetal aneuploidy. Still UNDERage at 18: trisomy 18 = ↓ AFP, ↓ estriol, ↓β-hCG, ↓ inhibin A. Table 2.11-2 outlines a typical prenatal diagnostic testing schedule by week. The sections that follow describe each recommended screening modality in further detail. The standard for diagnosing pregnancy. Produced by the placenta; peaks at 100,000 mIU/mL by 10 weeks of gesta tion. ■↓ throughout the second trimester; levels off in the third trimester. hCG levels double approximately every 48 hours during early pregnancy. This is often used to diagnose ectopic pregnancy when doubling is abnormal. Maternal serum α-fetoprotein (MSAFP), which is produced by the fetus, crosses the placenta in small amounts and enters the maternal circulation. Measurement results are reported as multiples of the median (MoMs) and depend on accurate gestational dating.


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First_Aid_Step2. Elevated MSAFP (> 2.5 MoMs): Associated with open neural tube defects (anencephaly, spina bifda), abdominal wall defects (gastroschisis, omphalocele), multiple gestation, incorrect gestational dating, fetal death, and placental abnormalities (e.g., placental abruption). Decreased MSAFP (< 0.5 MoM): Associated with trisomy 21 and 18, fetal demise, and inaccurate gestational dating. MSAFP is now rarely performed alone because its sensitivity for detecting chromosomal abnormalities is ↑ by adding inhibin A to estriol, β-hCG, and MSAFP (quad screening). Results of quad screening are as follows: gradually increases an addi tional 10% by 28 weeks. Peripheral venous Progressive increase to term. distention Peripheral vascular Progressive decrease to term. +40 resistance +30 Pulmonary Respiratory rate Unchanged. +20 Respiratory rate, vital capacity Tidal volume Increases by 30–40%. Expiratory reserve Gradual decrease. Vital capacity Unchanged. +10


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First_Aid_Step2. Pulmonary Respiratory rate Unchanged. +20 Respiratory rate, vital capacity Tidal volume Increases by 30–40%. Expiratory reserve Gradual decrease. Vital capacity Unchanged. +10 Respiratory minute Increases by 40%. volume ElectrolytesElectrolytes Unchanged. 0 second trimester. +20Hematocrit Decreases slightly. +10Fibrinogen Increases. Gastrointestinal Sphincter tone Decreases. 0 Gastric emptying Increases. time (Reproduced, with permission, from Gardner DG, Shoback D. Greenspan’s Basic & Clinical Endocrinology, 8th ed. New York: McGraw-Hill, 2007: Fig. 17-2B.) TABLE 2.11-1. Standard Prenatal Care


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First_Aid_Step2. Weight gain Guidelines for weight gain in pregnancy: ■Recommended gain: An additional 100–300 kcal/day; 500 kcal/day during breastfeeding. ■Excessive gain: > 1.5 kg/mo. ■Inadequate gain: < 1 kg/mo. Guidelines according to prepregnancy body mass index (BMI): ■Underweight (BMI < 19.8): 12–18 kg gain. ■Acceptable (BMI 19.8–26.0): 11–16 kg gain. ■Overweight (BMI 26.1–29.0): 7–11 kg gain. ■Severely overweight (BMI > 29.0): 7 kg gain. Nutrition Guidelines for nutritional supplementation: ■Folic acid supplements (↓ neural tube defects for all reproductive-age women): 0.4 mg/day, or 4 mg/day for women with a history of neural tube defects in prior pregnancies. ■Iron: Starting at the frst visit, 30 mg/day of elemental iron (or 150 mg of iron sulfate). ■Calcium: 1300 mg/day for women < 19 years of age; 1000 mg/day for those > 19 years of age. Additional guidelines for complete vegetarians: ■Vitamin D: 10 μg or 400 IU/day. ■Vitamin B12: 2 μg/day. Exercise Thirty minutes of moderate exercise


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First_Aid_Step2. of age; 1000 mg/day for those > 19 years of age. Additional guidelines for complete vegetarians: ■Vitamin D: 10 μg or 400 IU/day. ■Vitamin B12: 2 μg/day. Exercise Thirty minutes of moderate exercise daily is recommended.


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First_Aid_Step2. Trisomy 18: All four are ↓. Trisomy 21: ↓ AFP and estriol; ↑ β-hCG and inhibin A. 2 up, 2 down: trisomy 21 = ↓ AFP, ↓ estriol, ↑β-hCG, ↑ inhibin A. Recommended at weeks 9–14. Pregnancy-associated plasma protein A (PAPP-A) + ultrasound-determined nuchal transparency (a measure of fuid in the fetal neck) + free β-hCG can detect ~85% of cases of Down syndrome and ~97% of cases of trisomy 18. Advantages: Screen of low-risk pregnant women (< 35 years of age); available earlier and less invasive than chorionic villus sampling (see below). Recommended at weeks 10–12. Involves transcervical or transabdominal aspiration of placental (chorionic villi) tissue. Advantages: Has a diagnostic accuracy comparable to that of amniocentesis; available at 10–12 weeks’ gestation. Disadvantages: Carries a risk of fetal loss (1–2%); cannot detect open neural tube defects. Limb defects have been associated with CVS performed at ≤ 9 weeks. T AB LE 2.1 1 -2. Prenatal Diagnostic Testing Schedule


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First_Aid_Step2. Limb defects have been associated with CVS performed at ≤ 9 weeks. T AB LE 2.1 1 -2. Prenatal Diagnostic Testing Schedule Prenatal visits Weeks 0–28: Every four weeks. Weeks 29–35: Every two weeks. Weeks 36–birth: Every week. Initial visit 9–14 weeks Offer PAPP-A + nuchal transparency + free β-hCG +/– CVS. 15–20 weeks Offer MSAFP or quad screen (AFP, estriol, β-hCG, and inhibin A) +/– amniocentesis. 18–20 weeks Ultrasound for full anatomic screen. 24–28 weeks One-hour glucose challenge test for gestational diabetes screen. Heme: CBC, Rh factor, type and screen. Infectious disease: UA and culture, rubella antibody titer, HBsAg, RPR/VDRL, cervical gonorrhea and chlamydia, PPD, HIV, Pap smear (to check for dysplasia). If indicated: HbA1c, sickle cell screening. Discuss genetic screening: Tay-Sachs, CF. Recommended at 15–20 weeks. Consists of transabdominal aspiration of amniotic fuid using an ultrasound-guided needle and evaluation of fetal cells for genetic studies.


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First_Aid_Step2. Recommended at 15–20 weeks. Consists of transabdominal aspiration of amniotic fuid using an ultrasound-guided needle and evaluation of fetal cells for genetic studies. Advantages: Detects ~80% of open neural tube defects, ~85% of cases of Down syndrome, and ~60% of cases of trisomy 18. Disadvantages: Risks include premature rupture of membranes (PROM), chorioamnionitis, and fetal-maternal hemorrhage, which can result in fetal loss (0.5%). Indicated for the following: In women who will be > 35 years of age at the time of delivery. In conjunction with an abnormal quad screen. In Rh-sensitized pregnancy to obtain fetal blood type or to detect fetal hemolysis. To evaluate fetal lung maturity via a lecithin-to-sphingomyelin ratio ≥ 2.5 or to detect the presence of phosphatidylglycerol (done during the third trimester).


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First_Aid_Step2. To evaluate fetal lung maturity via a lecithin-to-sphingomyelin ratio ≥ 2.5 or to detect the presence of phosphatidylglycerol (done during the third trimester). Major defects are apparent in about 3% of births and in roughly 4.5% of children by f ve years of age. Table 2.11-3 lists FDA risk classif cations of pharmaceutical products for use during pregnancy. Table 2.11-4 outlines common teratogenic agents. T AB LE 2.1 1 -3. FDA Risk Classifcation of Drugs for Use During Pregnancy


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First_Aid_Step2. Category A Adequate and well-controlled studies in women fail to demonstrate a risk to the fetus in the frst trimester (and there is no risk in later trimesters). The possibility of fetal harm seems remote. Vitamin B6, vitamin E, folic acid (within the recommended daily allowances). Category B Either animal reproduction studies have not demonstrated risk to the fetus but no adequate and well-controlled studies in pregnant women have been reported, or animal reproduction studies have shown an adverse effect that was not confrmed in controlled studies in women in the frst trimester (and there is no evidence of risk in later trimesters). Ampicillin, acetaminophen, bupropion. Category C Either studies in animals have revealed adverse effects on the fetus but no controlled studies in women have been reported, or studies in women and animals are not available. Drugs should be given only if the potential benef t justifes the potential risk to the fetus. Diphenhydramine, rifampin, zidovudine


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First_Aid_Step2. been reported, or studies in women and animals are not available. Drugs should be given only if the potential benef t justifes the potential risk to the fetus. Diphenhydramine, rifampin, zidovudine (AZT). Category D Positive evidence of human fetal risk exists, but the benefts from use in pregnant women may be acceptable despite the risk. Alcohol, phenytoin, tetracycline. Category X Studies in animals or humans have demonstrated fetal abnormalities, or evidence exists of fetal risk based on human experience, or both, and the risk in pregnant women clearly outweighs any possible benef t. Isotretinoin, thalidomide, warfarin.


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First_Aid_Step2. Pregnant women should not change the cat’s litterbox. First-trimester toxoplasmosis infection is less common but more severe. Third-trimester infection is more common but less severe. May occur at any time during pregnancy, labor, and delivery. Common sequelae include premature delivery, CNS abnormalities, anemia, jaundice, hepatosplenomegaly, and growth retardation. The most common pathogens can be remembered through use of the mnemonic TORCHeS (see also Table 2.11-5): Toxoplasmosis: Transplacental transmission, with 1° infection occurring via consumption of raw meat or contact with cat feces. Specif c f ndings include hydrocephalus, intracranial calcifications, chorioretinitis, and ring-enhancing lesions on head CT. Other: Parvovirus, varicella, Listeria, TB, malaria, fungi. Rubella: Transplacental transmission in the frst trimester. Specif c f ndings include a purpuric “blueberry muffin” rash, cataracts, mental retardation, hearing loss, and patent ductus arteriosus (PDA).


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First_Aid_Step2. CMV: The most common congenital infection; primarily transmitted transplacentally. Specif c fndings include a petechial rash (similar to “blueberry muffn” rash) and periventricular calcifications. Herpes: Intrapartum transmission if the mother has active lesions. Can cause skin, eye, and mouth infections or life-threatening CNS/systemic infection. HIV: Transmission can occur in utero, at the time of delivery, or via breast milk. Occurs in 13–39% of births to infected mothers. The combination of AZT treatment (prenatally, intrapartum, and neonatally for the f rst six weeks of life) and cesarean delivery can lower transmission to 2%. Newborns with congenitally acquired HIV are often asymptomatic. Failure to T AB LE 2.1 1 -4. Common Teratogenic Agents and Their Associated Defects


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First_Aid_Step2. ACEIs Fetal renal tubular dysplasia and neonatal renal failure, oligohydramnios, intrauterine growth restriction (IUGR), lack of cranial ossif cation. Alcohol Fetal alcohol syndrome (growth restriction before and after birth, mental retardation, midfacial hypoplasia, renal and cardiac defects). Consumption of > 6 drinks per day is associated with a 40% risk of fetal alcohol syndrome. Androgens Virilization of females; advanced genital development in males. Carbamazepine Neural tube defects, fngernail hypoplasia, microcephaly, developmental delay, IUGR. Cocaine Bowel atresias; congenital malformations of the heart, limbs, face, and GU tract; microcephaly; IUGR; cerebral infarctions. Diethylstilbestrol (DES) Clear cell adenocarcinoma of the vagina or cervix, vaginal adenosis, abnormalities of the cervix and uterus or testes, possible infertility. Lead ↑ spontaneous abortion (SAB) rate; stillbirths. Lithium Congenital heart disease (Ebstein’s anomaly). Methotrexate ↑ SAB rate. Organic


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First_Aid_Step2. of the cervix and uterus or testes, possible infertility. Lead ↑ spontaneous abortion (SAB) rate; stillbirths. Lithium Congenital heart disease (Ebstein’s anomaly). Methotrexate ↑ SAB rate. Organic mercury Cerebral atrophy, microcephaly, mental retardation, spasticity, seizures, blindness. Phenytoin IUGR, mental retardation, microcephaly, dysmorphic craniofacial features, cardiac defects, f ngernail hypoplasia. Radiation Microcephaly, mental retardation. Medical diagnostic radiation delivering < 0.05 Gy to the fetus has no teratogenic risk. Streptomycin and kanamycin Hearing loss; CN VIII damage. Tetracycline Permanent yellow-brown discoloration of deciduous teeth; hypoplasia of tooth enamel. Thalidomide Bilateral limb defciencies, anotia and microtia, cardiac and GI anomalies. Trimethadione and paramethadione Cleft lip or cleft palate, cardiac defects, microcephaly, mental retardation. Valproic acid Neural tube defects (spina bifda); minor craniofacial defects. Vitamin A and


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First_Aid_Step2. and paramethadione Cleft lip or cleft palate, cardiac defects, microcephaly, mental retardation. Valproic acid Neural tube defects (spina bifda); minor craniofacial defects. Vitamin A and derivatives ↑ SAB rate, microtia, thymic agenesis, cardiovascular defects, craniofacial dysmorphism, microphthalmia, cleft lip or cleft palate, mental retardation. Warfarin (wages war on the fetus) Nasal hypoplasia and stippled bone epiphyses, developmental delay, IUGR, ophthalmologic abnormalities.


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First_Aid_Step2. T AB LE 2.1 1 -5. Diagnosis and Treatment of Common Congenital Infections


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First_Aid_Step2. Toxoplasmosis Serologic testing Pyrimethamine + sulfadiazine Avoid exposure to cat feces during pregnancy. Spiramycin prophylaxis for the third trimester. Rubella Serologic testing Immunize before pregnancy; vaccinate the mother after delivery if serologic titers remain . CMV Urine culture, PCR of amniotic f uid Postpartum ganciclovir HSV Serologic testing Acyclovir Perform a C-section if lesions are present at delivery. ELISA, Western blot AZT or nevirapine in pregnant women with HIV; perform elective C-section if viral load is > 1000; treat infants with prophylactic AZT; avoid breastfeeding. Dark-f eld microscopy, VDRL/RPR, FTA-ABS Penicillin Penicillin in pregnant women who test . HIV Syphilis thrive, bacterial infections with common organisms, and an ↑ incidence of upper and lower respiratory diseases may appear early or may be delayed for months to years. HIV-mothers should be counseled not to breastfeed their infants.


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First_Aid_Step2. Syphilis: Primarily intrapartum transmission. Specif c fndings include a maculopapular skin rash, lymphadenopathy, hepatomegaly, “snufﬂ es” (mucopurulent rhinitis), and osteitis. In childhood, late congenital syphilis is characterized by saber shins, saddle nose, CNS involvement, and Hutchinson’s triad: peg-shaped upper central incisors, deafness, and interstitial keratitis (photophobia, lacrimation). Defned as loss of products of conception (POC) prior to the 20th week of pregnancy. Approximately 60% of chemically evident pregnancies and 15– 20% of clinically diagnosed pregnancies terminate in a SAB. More than 80% will occur in the frst trimester. Risk factors are as follows: Chromosomal abnormalities: A factor in approximately 50% of SABs in the frst trimester, 20–30% in second-trimester losses, and 5–10% in third-trimester losses. Maternal factors: Maternal trauma, ↑ maternal age, infection, dietary def ciencies.


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First_Aid_Step2. Maternal factors: Maternal trauma, ↑ maternal age, infection, dietary def ciencies. Inherited thrombophilias: Factor V Leiden, prothrombin, antithrombin, proteins C and S, methylene tetrahydrofolate reductase (hyperhomocysteinemia). Immunologic issues: Antiphospholipid antibodies, alloimmune factors. Anatomic issues: Uterine abnormalities, incompetent cervix, cervical conization or loop electrosurgical excision procedure (LEEP), cervical injury, DES exposure, anatomical abnormalities of the cervix. Endocrinologic issues: Diabetes mellitus (DM), hypothyroidism, progeste rone def ciency. Environmental factors: Tobacco (with > 14 cigarettes/day, the risk is twofold), alcohol, caffeine (> 500 mg caffeine/day), toxins, drugs, radiation. Fetal factors: Anatomic malformation. See Table 2.11-6 for types of SAB. ■↓ levels of hCG. Ultrasound: Can identify the gestational sac 5–6 weeks from the LMP, a fetal pole at six weeks, and fetal cardiac activity at 6–7 weeks.


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First_Aid_Step2. See Table 2.11-6 for types of SAB. ■↓ levels of hCG. Ultrasound: Can identify the gestational sac 5–6 weeks from the LMP, a fetal pole at six weeks, and fetal cardiac activity at 6–7 weeks. With accurate dating, a small, irregular intrauterine sac without a fetal pole on transvaginal ultrasound is diagnostic of an abnormal pregnancy. Maternal Rh type should be determined and RhoGAM given if the type is Rh . It has been estimated that 50% of all pregnancies in the United States are unintended. Some 25% of all pregnancies end in elective abortion. Options for elective abortion depend on GA and patient preferences (see Table 2.11-7). Leopold’s maneuvers are used to determine fetal lie (longitudinal or transverse) and, if possible, fetal presentation (breech or cephalic). Cervical examination:


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First_Aid_Step2. Leopold’s maneuvers are used to determine fetal lie (longitudinal or transverse) and, if possible, fetal presentation (breech or cephalic). Cervical examination: Evaluate dilation, effacement, station, cervical position, and cervical consistency. Use the Bishop score (see Table 2.11-8) to evaluate the favorability of delivery and the probability of succeeding with an induction. Scoring is interpreted as follows: 0–4: Indicates a 45–50% chance of failure. Give prostaglandins for induction. 5–9: Points to a 10% chance of failure. Give pitocin for induction. 10–13: Associated with a very high probability of success. There is no need for intervention for induction. Confrm or determine fetal presentation. Determine fetal position through palpation of the fetal sutures and fontanelles. Conduct a sterile speculum exam if rupture of membranes (ROM) is suspected. Table 2.11-9 and Figure 2.11-4 depict the normal stages of labor.


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First_Aid_Step2. Conduct a sterile speculum exam if rupture of membranes (ROM) is suspected. Table 2.11-9 and Figure 2.11-4 depict the normal stages of labor. FHR monitoring is the most common obstetric procedure and is used in 85% of live births in the United States. It may be performed with an electrode at T AB LE 2.1 1 -6. Types of Spontaneous Abortion


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First_Aid_Step2. Complete POC is expelled. Pain ceases, but spotting may persist. Closed os. Ultrasound shows an empty uterus. POC should be sent to pathology to conf rm fetal tissue. None. Incomplete Some POC is expelled. Bleeding/mild cramping. Visible tissue on exam. Open os. Ultrasound shows retained fetal tissue. Manual uterine aspiration (MUA) or D&C. Threatened No POC is expelled. Uterine bleeding +/– abdominal pain. Closed os + intact membranes + fetal cardiac motion on ultrasound. Pelvic rest for 24–48 hours and follow-up ultrasound to assess the viability of conceptus. Inevitable No POC is expelled. Uterine bleeding and cramps. Open os +/− ROM. MUA, D&C, misoprostol, or expectant management. Missed No POC is expelled. No fetal cardiac motion. No uterine bleeding. Brownish vaginal discharge. Closed os. No fetal cardiac activity; retained fetal tissue on ultrasound. MUA, D&C, or misoprostol. Septic Endometritis leading to septicemia. Maternal mortality is 10–15%. Hypotension, hypothermia, ↑


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First_Aid_Step2. os. No fetal cardiac activity; retained fetal tissue on ultrasound. MUA, D&C, or misoprostol. Septic Endometritis leading to septicemia. Maternal mortality is 10–15%. Hypotension, hypothermia, ↑ WBC count. MUA, D&C, and IV antibiotics. Intrauterine fetal demise Absence of fetal cardiac activity. Uterus small for GA; no fetal heart tones or movement on ultrasound. Induce labor; evacuate the uterus (D&E) to prevent DIC at GA > 16 weeks. Recurrenta If early in pregnancy, often due to chromosomal abnormalities. If later in pregnancy, often due to hypercoagulable states (e.g., SLE, factor V Leiden, protein S def ciency). Incompetent cervix should be suspected with a history of painless dilation of the cervix and delivery of a normal fetus between 18 and 32 weeks. Karyotyping of both parents. Hypercoagulability workup of mother. Evaluate for uterine abnormalities. Surgical cerclage procedures to suture the cervix closed until labor or ROM occurs with subsequent removal prior to delivery.


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First_Aid_Step2. Hypercoagulability workup of mother. Evaluate for uterine abnormalities. Surgical cerclage procedures to suture the cervix closed until labor or ROM occurs with subsequent removal prior to delivery. Restriction of activities. a Defned as two or more consecutive SABs or a total of three SABs in one year.


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First_Aid_Step2. tached to the fetal scalp (a method that yields more precise results), or external monitoring can be conducted using Doppler ultrasound (a less invasive option). However, continuous electronic FHR monitoring has not been shown to be more effective than appropriate intermittent monitoring. TABLE 2.11-7. Elective Termination of Pregnancy First trimester (90% therapeutic abortions [TABs]) Medical management: ■Oral mifepristone (low dose) + oral/vaginal misoprostol ■IM/oral methotrexate + oral/vaginal misoprostol ■Vaginal or sublingual or buccal misoprostol (high dose), repeated up to three times Surgical management: ■ Manual aspiration ■D&C with vacuum aspiration Up to: 49 days’ GA 49 days’ GA 56 days’ GA Up to 13 weeks’ GA Second trimester (10% TABs) Obstetric management: Induction of labor (typically with prostaglandins, amniotomy, and oxytocin) Surgical management: D&E 13–24 weeks’ GA (depending on state laws) Same as above


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First_Aid_Step2. Patients without complications: Review FHR tracings every 30 minutes in the frst stage of labor and every 15 minutes in the second stage of labor. Patients with complications: Review FHR tracings every 15 minutes in the frst stage of labor and every 5 minutes in the second stage of labor. Rate (normal = 110–160 bpm): FHR < 110 bpm: Bradycardia. Can be caused by congenital heart malformations or severe hypoxia (2° to uterine hyperstimulation, cord prolapse, or rapid fetal descent). FHR > 160 bpm: Tachycardia. Can be caused by hypoxia, maternal fever, or fetal anemia. Variability (normal beat-to-beat variability = 6–25 bpm): See Figures 2.11-5 and 2.11-6. Undetectable variability: Indicates severe fetal distress. TABLE 2.11-8. Bishop Score TABLE 2.11-9. Stages of Labor


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First_Aid_Step2. Undetectable variability: Indicates severe fetal distress. TABLE 2.11-8. Bishop Score TABLE 2.11-9. Stages of Labor First Latent Active Onset of labor to 3–4 cm dilation 4 cm to complete cervical dilation (10 cm) 6–11 hrs 4–6 hrs (1.2 cm/hr) 4–8 hrs 2–3 hrs (1.5 cm/hr) Prolongation seen with excessive sedation and hypertonic uterine contractions. Prolongation seen with cephalopelvic disproportion. Second Complete cervical dilation to delivery of infant 0.5–3.0 hrs 5–30 min Baby goes through all cardinal movements of delivery. Third Delivery of infant to delivery of placenta 0–0.5 hr 0–0.5 hr Uterus contracts and placenta separates to establish hemostasis. Minimal variability: < 6 bpm. Indicates fetal distress or the effects of opioids or magnesium. Normal variability: 6–25 bpm. Marked variability: > 25 bpm. May indicate fetal distress; may occur before a ↓ in variability. Sinusoidal variability: Points to serious fetal anemia; may also occur during maternal meperidine use.


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First_Aid_Step2. Sinusoidal variability: Points to serious fetal anemia; may also occur during maternal meperidine use. FIGURE 2.11-4. Stages of labor. Cervical dilation, level of descent, and orientation of occipitoanterior presentation during various stages of labor. (Reproduced, with permission, from DeCherney AH. Current Obstetric & Gynecologic Diagnosis & Treatment, 8th ed. Stamford, CT: Appleton & Lange, 1994: 211.) F IGU R E 2.1 1 -5. Varying (variable) fetal heart rate decelerations. Deceleration B exhibits “shoulders” of acceleration compared with deceleration A. (Reproduced, with permission, from Cunningham FG et al. Williams Obstetrics, 22nd ed. New York: McGraw-Hill, 2005: Fig. 18-21.) F IGU R E 2.1 1 -6. Late fetal heart rate decelerations.


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First_Aid_Step2. F IGU R E 2.1 1 -6. Late fetal heart rate decelerations. Late decelerations due to uteroplacental insuffciency resulting from placental abruption. Immediate cesarean delivery was performed. Umbilical artery pH was 7.05 and PO2 was 11 mmHg. (Reproduced, with permission, from Cunningham FG et al. Williams Obstetrics, 22nd ed. New York: McGraw-Hill, 2005: Fig. 18-17.) Accelerations: Onset of an ↑ in FHR to a peak in < 30 seconds. Reassuring because they indicate fetal ability to appropriately respond to the environment. Decelerations: See Table 2.11-10. In general, antepartum fetal surveillance is used in pregnancies in which the risk of antepartum fetal demise is ↑. Testing is initiated in most at-risk patients TABLE 2.11-10. Types of Fetal Deceleration


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First_Aid_Step2. TABLE 2.11-10. Types of Fetal Deceleration Early A visually apparent, gradual (onset to nadir in > 30 sec) ↓ in FHR with a return to baseline that mirrors the uterine contraction. Head compression from the uterine contraction (normal). Late A visually apparent, gradual (onset to nadir in > 30 sec) ↓ in FHR with return to baseline whose onset, nadir, and recovery occur after the beginning, peak, and end of uterine contraction, respectively. Uteroplacental insuff ciency and fetal hypoxemia. Variable An abrupt (onset to nadir in < 30 sec), visually apparent ↓ in FHR below baseline lasting ≥ 15 sec but < 2 min. Umbilical cord compression. Illustrations reproduced, with permission, from Cunningham FG et al. Williams Obstetrics, 22nd ed. New York: McGraw-Hill, 2005: Figs.18-14, 18-16, and 18-18. at 32–34 weeks (or 26–28 weeks if there are multiple worrisome risk factors present). The following assessments are made:


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First_Aid_Step2. at 32–34 weeks (or 26–28 weeks if there are multiple worrisome risk factors present). The following assessments are made: Fetal movement assessment: Assessed by the mother as the number of fetal movements over one hour. The average time to obtain 10 movements is 20 minutes. Maternal reports of ↓ fetal movements should be evaluated by means of the tests described below. Nonstress test (NST): Performed with the mother resting in the lateral tilt position (to prevent supine hypotension). FHR is monitored externally by Doppler along with a tocodynamometer to detect uterine contractions. Acoustic stimulation may be used. “Reactive” (normal response): Two accelerations of ≥ 15 bpm above baseline lasting for at least 15 seconds over a 20-minute period (see Figure 2.11-7).


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First_Aid_Step2. “Reactive” (normal response): Two accelerations of ≥ 15 bpm above baseline lasting for at least 15 seconds over a 20-minute period (see Figure 2.11-7). “Nonreactive”: Fewer than two accelerations over a 20-minute period. Perform further tests (e.g., a biophysical profle). Lack of FHR accelerations may occur with any of the following: GA < 32 weeks, fetal sleeping, fetal CNS anomalies, and maternal sedative or narcotic administration. Contraction stress test (CST): Performed in the lateral recumbent position. FHR is monitored during spontaneous or induced (via nipple stimulation or oxytocin) contractions. Reactivity is determined from fetal heart monitoring, as with the NST. The procedure is contraindicated in women with preterm membrane rupture or known placenta previa; women with a history of uterine surgery; and women who are at high risk for preterm labor. FIGURE 2.11-7. Reactive nonstress test.


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First_Aid_Step2. FIGURE 2.11-7. Reactive nonstress test. (Reproduced, with permission, from Cunningham FG et al. Williams Obstetrics, 22nd ed. New York: McGraw-Hill, 2005: Fig. 15-7.) A negative CST is good; a positive one is bad. When performing a BPP, remember to– Test the Baby, MAN! “Positive” CST: Defned by late decelerations following 50% or more of contractions in a 10-minute window; raises concerns about fetal compromise. Delivery is usually warranted. “Negative” CST: Defned as no late or signifcant variable decelerations within 10 minutes and at least three contractions. Highly predictive of fetal well-being in conjunction with a normal NST. “Equivocal” CST: Def ned by intermittent late decelerations or significant variable decelerations. Biophysical profile (BPP): Uses real-time ultrasound to assign a score of 2 (normal) or 0 (abnormal) to fve parameters: fetal tone, breathing, movement, amniotic fuid volume, and NST. Scoring is as follows: 8–10: Reassuring for fetal well-being.


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First_Aid_Step2. 6: Considered equivocal. Term pregnancies are usually delivered with this prof le. 0–4: Extremely worrisome for fetal asphyxia; strong consideration should be given to immediate delivery if no other explanation is found. Modified biophysical profile (mBPP): Combines the NST with the amniotic fuid index (AFI, or the sum of the measurements of the deepest cord-free amniotic fuid measured in each of the abdominal quadrants). The test is considered normal with a reactive NST and an AFI > 5 cm. Umbilical artery Doppler velocimetry: With IUGR, there is reduction and even reversal of umbilical artery diastolic fow. The test is of benef t only when IUGR is suspected. Oligohydramnios (AFI < 5 cm) always warrants further workup.


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First_Aid_Step2. Oligohydramnios (AFI < 5 cm) always warrants further workup. Uterine contractions and cervical dilation result in visceral pain (T10–L1). Descent of the fetal head and pressure on the vagina and perineum result in somatic pain (pudendal nerve, S2–S4). In the absence of a medical contraindication, maternal request is a suffcient medical indication for pain relief during labor. Absolute contraindications to regional anesthesia (epidural, spinal, or combination) include the following (see also Table 2.11-11): Maternal use of a once-daily dose of low-molecular-weight heparin (LMWH) within 12 hours Skin infection over the site of needle placement ■↑ ICP caused by a mass lesion If “morning sickness” persists after the f rst trimester, think hyperemesis gravidarum.


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First_Aid_Step2. Skin infection over the site of needle placement ■↑ ICP caused by a mass lesion If “morning sickness” persists after the f rst trimester, think hyperemesis gravidarum. Persistent vomiting not related to other causes, acute starvation (usually large ketonuria), and weight loss (usually at least a 5% ↓ from prepregnancy weight). Occurs in 0.5–2.0% of pregnancies. More common in f rst pregnancies, multiple gestations, and molar pregnancies. ↑β-hCG and ↑ estradiol have been implicated in its pathophysiology. T AB LE 2.1 1 -1 1. Available Methods of Anesthesia and Analgesia


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First_Aid_Step2. Nonpharmacologic (social support, massages, breathing, aromatherapy, ambulation and repositioning) No known side effects. Works by increasing coping with pain rather than eliminating pain. Limited pain relief. Opioids Provide an adequate level of pain relief for some women without the risks associated with regional anesthesia. Local block (lidocaine) Excellent anesthesia before episiotomy and during repair of lacerations; can be used to perform a pudendal block. Rarely, may cause seizures, hypotension, and cardiac arrhythmias. Epidural The most effective form of pain relief; can also be used for cesarean delivery or postpartum tubal ligation. Can result in pruritus, fever, hypotension, and transient FHR deceleration. Spinal Rapid-onset analgesia that provides excellent pain relief for procedures of limited duration (30–250 minutes). Limited duration; puts patients at risk for hypotension, postdural puncture headache, and transient neurologic symptoms. Combined spinal epidural General


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First_Aid_Step2. Offers rapid onset of spinal analgesia combined with the ability to prolong the duration of analgesia with continuous epidural infusion. Used in emergent cesarean delivery and indicated in some cases of FHR abnormality; can be useful in cases where regional anesthesia is absolutely contraindicated or fails. The sedative effect of opioids ↓ FHR variability and ↑ the possible need for neonatal naloxone administration and f ve-minute Apgar scores < 7. Carries the risks of both procedures; may ↑ the risk of bradycardia and emergent cesarean delivery over epidural analgesia alone. Requires airway control; carries a signif cant risk of maternal aspiration and neonatal depression (inhaled anesthetic agents readily cross the placenta); associated with higher maternal morbidity rates than epidural anesthesia. Distinguish from “morning sickness,” acid refux, gastroenteritis, hyperthyroidism, and neurologic conditions. Rule out molar pregnancy: Check β-hCG level and ultrasound.


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First_Aid_Step2. Distinguish from “morning sickness,” acid refux, gastroenteritis, hyperthyroidism, and neurologic conditions. Rule out molar pregnancy: Check β-hCG level and ultrasound. Determine severity: Evaluate for ketonemia, ketonuria, hyponatremia, and hypokalemic, hypochloremic metabolic alkalosis. Measure liver enzymes, serum bilirubin, and serum amylase/lipase. The f rst step in the diagnosis of hyperemesis gravidarum is to rule out molar pregnancy with ultrasound +/– β-hCG. The f rst step in the management of hyperemesis gravidarum is vitamin B6 and doxylamine if not severe or antiemetics and IV f uids if severe. Gestational diabetes is typically asymptomatic, so the f rst step in diagnosis is a one-hour glucose challenge at 24–28 weeks. If ≥ 140 mg/dL, perform a three-hour glucose challenge test. Keys to the management of gestational diabetes: (1) the ADA diet; (2) insulin if needed; (3) ultrasound for fetal growth; and (4) NST beginning at 30–32 weeks.


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First_Aid_Step2. Keys to the management of gestational diabetes: (1) the ADA diet; (2) insulin if needed; (3) ultrasound for fetal growth; and (4) NST beginning at 30–32 weeks. First step: Administer vitamin B6. Second step: Doxylamine (an antihistamine) PO. Third step: Promethazine or dimenhydrinate PO/PR. If severe: Metoclopramide, ondansetron, prochlorperazine, or promethazine IM/PO. If dehydrated: IV fuids, IV nutritional supplementation, and dimenhydrinate IV. Diabetes in pregnancy is divided into two categories: gestational diabetes, in which onset occurs during pregnancy, and pregestational diabetes. The White classif cation (see Table 2.11-12) is commonly used to classify women according to the nature of their diabetes and the associated risk. Carbohydrate intolerance of variable severity that is frst diagnosed during pregnancy. Occurs in 3–5% of all pregnancies, usually in late pregnancy.


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First_Aid_Step2. Carbohydrate intolerance of variable severity that is frst diagnosed during pregnancy. Occurs in 3–5% of all pregnancies, usually in late pregnancy. Typically asymptomatic. Edema, polyhydramnios, or a large-for-GA infant (> 90th percentile) may be warning signs. First step: One-hour 50-g glucose challenge test; venous plasma glucose is measured one hour later (at 24–28 weeks). Values ≥ 140 mg/dL are considered abnormal. Next step: Confrm with an oral three-hour (100-g) glucose tolerance test showing any two of the following: fasting > 95 mg/dL; one hour > 180 mg/ dL; two hours > 155 mg/dL; three hours > 140 mg/dL. Mother: First step: Start with the ADA diet, regular exercise, and strict glucose monitoring (four times a day). Tight maternal glucose control (fasting glucose < 100; oneto two-hour postprandial glucose < 150) improves outcomes. Next step: Add insulin if dietary control is insuff cient. Give intrapartum insulin and dextrose to maintain tight control during delivery.


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First_Aid_Step2. Next step: Add insulin if dietary control is insuff cient. Give intrapartum insulin and dextrose to maintain tight control during delivery. Fetus: Obtain periodic ultrasound and NSTs to assess fetal growth and wellbeing. It may be necessary to induce labor at 39–40 weeks. More than 50% of patients go on to develop glucose intolerance and/or type 2 DM later in life. T AB LE 2.1 1 -1 2. White Classifcation of Diabetes in Pregnancy A1 Gestational diabetes; insulin not required. A2 Gestational diabetes; insulin required. B Age of onset 20 years or older or duration < 10 years. C Age of onset 10–19 years or duration 10–19 years. D Age of onset < 10 years or duration > 20 years. F Nephropathy. H Cardiomyopathy. R Proliferating retinopathy. RF Retinopathy and nephropathy. T Renal transplant.


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First_Aid_Step2. Observed in 1% of all pregnancies. Insulin requirements may ↑ as much as threefold. Poorly controlled DM is associated with an ↑ risk of congenital malformations, fetal loss, and maternal/fetal morbidity during labor and delivery. Mother: Renal, ophthalmologic, and cardiac evaluation to assess for end-organ damage. Strict glucose control (with diet, exercise, insulin therapy, and frequent self-monitoring for type 1 and type 2 DM) to minimize fetal defects. Fasting morning: ≤ 90 mg/dL. Two-hour postprandial: < 120 mg/dL. Fetus: 18–20 weeks: Ultrasound to determine fetal age and growth; evaluate for cardiac anomalies and polyhydramnios; quad screen to screen for developmental anomalies. 32–34 weeks: Close fetal surveillance (e.g., NST, CST, BPP). Admit if maternal DM has been poorly controlled or fetal parameters are a concern. Serial ultrasounds for fetal growth. Delivery and postpartum:


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First_Aid_Step2. Delivery and postpartum: Maintain normoglycemia (80–100 mg/dL) during labor with an IV insulin drip and hourly glucose measurements. Consider early delivery in the setting of poor maternal glucose control, preeclampsia, macrosomia, or evidence of fetal lung maturity. Cesarean delivery should be considered for an estimated fetal weight (EFW) > 4500 g. Greater than eight, investigate! If HbA1c is > 8%, look for congenital abnormalities. If UA before 20 weeks reveals glycosuria, think pregestational diabetes. Hyperglycemia in the f rst trimester suggests preexisting diabetes and should be managed as pregestational diabetes. Encourage breastfeeding with an appropriate ↑ in caloric intake. Continue glucose monitoring postpartum. Insulin needs rapidly ↓ after delivery. See Table 2.11-13. Distinguished as follows:


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First_Aid_Step2. Encourage breastfeeding with an appropriate ↑ in caloric intake. Continue glucose monitoring postpartum. Insulin needs rapidly ↓ after delivery. See Table 2.11-13. Distinguished as follows: Gestational hypertension (formerly known as pregnancy-induced hypertension): Idiopathic hypertension without signif cant proteinuria (< 300 mg/L) that develops at > 20 weeks’ gestation. As many as 25% of patients may go on to develop preeclampsia. Chronic hypertension: Present before conception and at < 20 weeks’ gestation, or may persist for > 12 weeks postpartum. Up to one-third of patients may develop superimposed preeclampsia. Tx: Monitor BP closely and treat with appropriate antihypertensives (e.g., methyldopa, labetalol, nifedipine). Do not give ACEIs or diuretics, as ACEIs are known to lead to uterine ischemia, and diuretics can aggravate low plasma volume to the point of uterine ischemia. Cx: Complications are similar to those of preeclampsia (see below). Distinguished as follows:


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First_Aid_Step2. Cx: Complications are similar to those of preeclampsia (see below). Distinguished as follows: Preeclampsia: New-onset hypertension (SBP ≥ 140 mmHg or DBP ≥ 90 mmHg) and proteinuria (> 300 mg of protein in a 24-hour period) occurring at > 20 weeks’ gestation. Eclampsia: New-onset grand mal seizures in women with preeclampsia. HELLP syndrome (hemolytic anemia, elevated liver enzymes, and low platelets): A variant of preeclampsia with a poor prognosis. ■The etiology is unknown, but clinical manifestations are explained by vasospasm leading to hemorrhage and organ necrosis.


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First_Aid_Step2. ■The etiology is unknown, but clinical manifestations are explained by vasospasm leading to hemorrhage and organ necrosis. T AB LE 2.1 1 -1 3. Complications of Pregestational Diabetes Mellitus macrosomia) and need for C-section Preterm labor Infection Polyhydramnios Postpartum hemorrhage Maternal mortality Macrosomia or IUGR Cardiac and renal defects Neural tube defects (e.g., sacral agenesis) Hypocalcemia Polycythemia Hyperbilirubinemia IUGR Hypoglycemia from hyperinsulinemia Respiratory distress syndrome (RDS) Birth injury (e.g., shoulder dystocia) Perinatal mortality ■Risk factors include nulliparity, African-American ethnicity, extremes of age (< 20 or > 35), multiple gestation, molar pregnancy, renal disease (due to SLE or type 1 DM), a family history of preeclampsia, and chronic hypertension. See Table 2.11-14 for the signs and symptoms of preeclampsia and eclampsia. The only cure for preeclampsia/eclampsia is delivery of the fetus. Preeclampsia:


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First_Aid_Step2. See Table 2.11-14 for the signs and symptoms of preeclampsia and eclampsia. The only cure for preeclampsia/eclampsia is delivery of the fetus. Preeclampsia: If the patient is close to term or preeclampsia worsens, induce delivery with IV oxytocin, prostaglandin, or amniotomy. If far from term, treat with modifed bed rest and expectant management. Severe preeclampsia: First step: Control BP with labetalol and/or hydralazine (goal < 160/110 with a DBP of 90–100 to maintain fetal blood f ow). Second step: Prevent seizures with continuous magnesium sulfate drip. Watch for signs of magnesium toxicity (loss of DTRs, respiratory paralysis, coma). Continue seizure prophylaxis for 24 hours postpartum. Treat magnesium toxicity with IV calcium gluconate. Third step: Deliver by induction or C-section when mother is stable. Eclampsia: First step: ABCs with supplemental O2.


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First_Aid_Step2. Third step: Deliver by induction or C-section when mother is stable. Eclampsia: First step: ABCs with supplemental O2. Second step: Seizure control/prophylaxis with magnesium. If seizures recur, give IV diazepam. Monitor magnesium blood levels and magnesium toxicity; monitor fetal status. Control BP (labetalol and/or hydralazine). Limit fuids; Foley for strict I/Os. T AB LE 2.1 1 -1 4. Presentation of Preeclampsia and Eclampsia Signs of severe preeclampsia are persistent headache or other cerebral or visual disturbances, persistent epigastric pain, and hyperreactive ref exes.


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First_Aid_Step2. Signs of severe preeclampsia are persistent headache or other cerebral or visual disturbances, persistent epigastric pain, and hyperreactive ref exes. Mild preeclampsia Usually asymptomatic. BP ≥ 140/90 on two occasions > 6 hours apart. Proteinuria (> 300 mg/24 hrs or 1–2 urine dipsticks). Edema. Severe preeclampsia BP > 160/110 on two occasions > 6 hours apart. Renal: Proteinuria (> 5 g/24 hrs or 3–4 urine dipsticks) or oliguria (< 500 mL/24 hrs). Cerebral changes: Headache, somnolence. Visual changes: Blurred vision, scotomata. Hyperactive ref exes/clonus. RUQ pain. Hemolysis, elevated liver enzymes, thrombocytopenia (HELLP syndrome). Eclampsia The most common signs preceding an eclamptic attack are headache, visual changes, and RUQ/epigastric pain. Seizures are severe if not controlled with anticonvulsant therapy. With third-trimester bleeding, think anatomically: Vagina: bloody show, trauma Cervix: cervical cancer, cervical/vaginal lesion


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First_Aid_Step2. With third-trimester bleeding, think anatomically: Vagina: bloody show, trauma Cervix: cervical cancer, cervical/vaginal lesion Placenta: placental abruption, placenta previa Fetus: fetal bleeding The classic triad of ectopic pregnancy PAVEs the way for diagnosis: ■Third step: Initiate delivery if the patient is stable and convulsions are controlled. Postpartum management is the same as that for preeclampsia. Seizures may occur antepartum (25%), intrapartum (50%), or postpartum (25%); most occur within 48 hours after delivery. Preeclampsia: Prematurity, fetal distress, stillbirth, placental abruption, seizure, DIC, cerebral hemorrhage, serous retinal detachment, fetal/ maternal death. Eclampsia: Cerebral hemorrhage, aspiration pneumonia, hypoxic encephalopathy, thromboembolic events, fetal/maternal death. Defned as any bleeding that occurs after 20 weeks’ gestation. Complicates 3–5% of pregnancies (prior to 20 weeks, bleeding is referred to as threatened abortion).


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First_Aid_Step2. Defned as any bleeding that occurs after 20 weeks’ gestation. Complicates 3–5% of pregnancies (prior to 20 weeks, bleeding is referred to as threatened abortion). The most common causes are placental abruption and placenta previa (see Table 2.11-15 and Figure 2.11-8). Other causes include other forms of abnormal placentation (e.g., placenta accreta), ruptured uterus, genital tract lesions, and trauma. Most often tubal, but can be abdominal, ovarian, or cervical. Presents with abdominal pain and vaginal spotting/bleeding, although some patients are asymptomatic. Associated with etiologies that cause scarring to the fallopian tubes, including a history of PID, pelvic surgery, DES use, or endometriosis. The differential includes surgical abdomen, abortion, ovarian torsion, PID, and ruptured ovarian cyst. Approach a woman of reproductive age presenting with abdominal pain as a ruptured ectopic pregnancy until proven otherwise. Proceed as follows:


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First_Aid_Step2. Approach a woman of reproductive age presenting with abdominal pain as a ruptured ectopic pregnancy until proven otherwise. Proceed as follows: First step: pregnancy test and a transvaginal ultrasound showing an empty uterus. Second step: Confrm with a serial hCG without appropriate hCG doubling. Medical treatment (methotrexate) is suffcient for small, unruptured tubal pregnancies. Surgical options for salpingectomy or salpingostomy with evacuation (laparoscopy vs. laparotomy). Tubal rupture and hemoperitoneum (an obstetric emergency). T AB LE 2.1 1 -1 5. Placental Abruption vs. Placenta Previa


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First_Aid_Step2. Premature (before delivery) separation of normally implanted placenta. Abnormal placental implantation: ■ Total: Placenta covers the cervical os. ■ Marginal: Placenta extends to the margin of the os. ■ Low-lying: Placenta is in close proximity to the os. 1 in 100. 1 in 200. Risk factors Hypertension, abdominal/pelvic trauma, tobacco or cocaine use, previous abruption, rapid decompression of an overdistended uterus, excessive stimulation. Prior C-sections, grand multiparity, advanced maternal age, multiple gestation, prior placenta previa. Symptoms Painful, dark vaginal bleeding that does not spontaneously cease. Abdominal pain, uterine hypertonicity. Fetal distress. Painless, bright red bleeding that often ceases in 1–2 hours with or without uterine contractions. Usually no fetal distress. Diagnosis Primarily clinical. Transabdominal/transvaginal ultrasound sensitivity is only 50%; look for retroplacental clot; most useful for ruling out previa. Transabdominal/transvaginal ultrasound


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First_Aid_Step2. Diagnosis Primarily clinical. Transabdominal/transvaginal ultrasound sensitivity is only 50%; look for retroplacental clot; most useful for ruling out previa. Transabdominal/transvaginal ultrasound sensitivity is > 95%; look for an abnormally positioned placenta. Pathophysiology Incidence


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First_Aid_Step2. Stabilize patients with mild abruption and a premature fetus; manage expectantly (hospitalize; start IV and fetal monitoring; type and cross blood; bed rest). Moderate to severe abruption: Immediate delivery (vaginal delivery with amniotomy if mother and fetus are stable and delivery is expected soon; C-section for maternal or fetal distress). No vaginal exam! Stabilize patients with a premature fetus; manage expectantly. Give tocolytics. Serial ultrasound to assess fetal growth; resolution of partial previa. Give betamethasone to help with fetal lung maturity. Deliver by C-section. Indications for delivery include labor, life-threatening bleeding, fetal distress, documented fetal lung maturity, and 36 weeks’ GA.


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First_Aid_Step2. Deliver by C-section. Indications for delivery include labor, life-threatening bleeding, fetal distress, documented fetal lung maturity, and 36 weeks’ GA. Hemorrhagic shock. ↑ risk of placenta accreta. Coagulopathy: DIC in 10%. Vasa previa (fetal vessels crossing the internal os). Recurrence risk is 5–16% and rises to 25% after Preterm delivery, PROM, IUGR, congenital two previous abruptions. anomalies. Fetal hypoxia. Recurrence risk is 4–8%. F IGU R E 2.1 1 -8. Placental implantation. (A) Normal placenta. (B) Low implantation. (C) Partial placenta previa. (D) Complete placenta previa. (Adapted, with permis sion, from DeCherney AH. Current Obstetric & Gynecologic Diagnosis & Treatment, 8th ed. Stamford, CT: Appleton & Lange, 1994: 404.) Defned as an EFW less than the 10th percentile for GA. Affected infants are commonly born to women with systemic diseases that lead to uteroplacental insuffciency (intrauterine infection, hypertension, anemia).


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First_Aid_Step2. Affected infants are commonly born to women with systemic diseases that lead to uteroplacental insuffciency (intrauterine infection, hypertension, anemia). Other risk factors include maternal substance abuse, placenta previa, and multiple gestations. First step: Diagnose by confrming serial fundal height measurements with ultrasound. Second step: Ultrasound the fetus for EFW (although as pregnancy advances, ultrasound fetal weight estimates become increasingly unreliable). First step: Explore the underlying etiology and correct if possible. If near due date: Administer steroids (e.g., betamethasone) to accelerate fetal lung maturity. Then: Perform fetal monitoring with NST, CST, BPP, and umbilical artery Doppler velocimetry. A nonreassuring status near term may prompt delivery. ↑ perinatal morbidity and mortality. Defned as a birth weight > 90th percentile. A common sequela of gestational diabetes.


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First_Aid_Step2. ↑ perinatal morbidity and mortality. Defned as a birth weight > 90th percentile. A common sequela of gestational diabetes. Dx: Diagnose by weighing the newborn at birth (prenatal diagnosis is imprecise). Tx: Planned cesarean delivery may be considered for an EFW > 5000 g in women without diabetes and for an EFW > 4500 g in women with diabetes. Cx: ↑ risk of shoulder dystocia (leading to brachial plexus injury and Erb-Duchenne palsy) as birth weight ↑. Defned as an AFI > 20 on ultrasound. May be present in normal pregnancies, but fetal chromosomal developmental abnormalities must be considered. Etiologies include maternal DM, multiple gestation, isoimmunization, pulmonary abnormalities (e.g., cystic lung malformations), fetal anomalies (e.g., duodenal atresia, tracheoesophageal fstula, anencephaly), and twin-twin transfusion syndrome. Hx/PE: Usually asymptomatic.


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First_Aid_Step2. Hx/PE: Usually asymptomatic. Dx: Fundal height greater than expected. Evaluation includes ultrasound for fetal anomalies, glucose testing for DM, and Rh screen. Tx: Etiology specif c. Cx: Preterm labor, fetal malpresentation, cord prolapse. An AFI < 5 cm on ultrasound. Usually asymptomatic, but IUGR or fetal distress may be present. Etiologies include fetal urinary tract abnormalities (e.g., renal agenesis, GU obstruction), chronic uteroplacental insuff ciency, and ROM. Dx: The sum of the deepest amniotic fuid pocket in all four abdominal quadrants on ultrasound. Tx: Rule out inaccurate gestational dates. Treat the underlying cause if possible. Cx: Associated with a 40-fold ↑ in perinatal mortality. Other complications include musculoskeletal abnormalities (e.g., clubfoot, facial distortion), pulmonary hypoplasia, umbilical cord compression, and IUGR.


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First_Aid_Step2. In this condition, fetal RBCs leak into the maternal circulation, and maternal anti-Rh IgG antibodies form that can cross the placenta, leading to hemolysis of fetal Rh RBCs (erythroblastosis fetalis). There is an ↑ risk among an Rh-women who have had a previous SAB or TAB as well as among those who have undergone a previous delivery with no RhoGAM given. Sensitized Rhmothers with titers > 1:16 should be closely monitored with serial ultrasound and amniocentesis for evidence of fetal hemolysis. In severe cases, initiate preterm delivery when fetal lungs are mature. Prior to delivery, intrauterine blood transfusions may be given to correct a low fetal hematocrit. If the mother is Rh at 28 weeks and the father is Rh or unknown, give RhoGAM (Rh immune globulin). If the baby is Rh , give RhoGAM postpartum.


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First_Aid_Step2. If the mother is Rh at 28 weeks and the father is Rh or unknown, give RhoGAM (Rh immune globulin). If the baby is Rh , give RhoGAM postpartum. Give RhoGAM to Rh-mothers who undergo abortion or who have had an ectopic pregnancy, amniocentesis, vaginal bleeding, or placenta previa/ placental abruption. Type and screen is critical; follow β-hCG closely and prevent pregnancy for one year. Hydrops fetalis occurs when fetal hemoglobin drops to < 7 g/dL. Other complications include fetal hypoxia and acidosis, kernicterus, prematurity, and death. A range of proliferative trophoblastic abnormalities that can be benign or malignant. Complete moles: Usually result from sperm fertilization of an empty ovum; 46,XX (paternally derived). Incomplete (partial) moles: Occur when a normal ovum is fertilized by two sperm (or a haploid sperm that duplicates its chromosomes); usually 69,XXY and contain fetal tissue.


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First_Aid_Step2. Incomplete (partial) moles: Occur when a normal ovum is fertilized by two sperm (or a haploid sperm that duplicates its chromosomes); usually 69,XXY and contain fetal tissue. Presents with f rst-trimester uterine bleeding (most common), hyperemesis gravidarum, preeclampsia/eclampsia at < 24 weeks, and uterine size greater than dates. Risk factors include extremes of age (< 20 or > 40 years) and a diet def cient in folate or beta-carotene. No fetal heartbeat is detected. Pelvic exam may reveal enlarged ovaries (bilateral theca-lutein cysts) or expulsion of grapelike molar clusters into the vagina. Labs show markedly ↑ serum β-hCG (usually > 100,000 mIU/mL), and pelvic ultrasound reveals a “snowstorm” appearance with no gestational sac or fetus present (see Figure 2.11-9). CXR may show lung metastases; D&C reveals “cluster-of-grapes” tissue (see Figure 2.11-10). FIGURE 2.11-9. Molar pregnancy.


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First_Aid_Step2. CXR may show lung metastases; D&C reveals “cluster-of-grapes” tissue (see Figure 2.11-10). FIGURE 2.11-9. Molar pregnancy. Transvaginal ultrasound shows a large, complex intrauterine mass with cystic regions that have the characteristic appearance of grapes.(Reproduced, with permission, from Tintinalli JE et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 6th ed. New York: McGraw-Hill, 2004: Fig. 113-27.) Evacuate the uterus and follow with weekly β-hCG. Treat malignant disease with chemotherapy (methotrexate or dactinomycin) and residual uterine disease with hysterectomy; chemotherapy and irradiation are highly effective for metastases. F IGU R E 2.1 1 -1 0. Gross specimen of hydatidiform mole.


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First_Aid_Step2. F IGU R E 2.1 1 -1 0. Gross specimen of hydatidiform mole. A complete or classical hydatidiform mole is characterized grossly by an abundance of edematous enlarged chorionic villi but no fetus or fetal membranes. There are theca-lutein cysts in both ovaries (arrows). (Reproduced, with permission, from Cunningham FG et al. Williams Obstetrics, 22nd ed. New York: McGraw-Hill, 2005: Fig.11-1.) Molar pregnancy may progress to malignant GTD, including invasive moles (10–15%) and choriocarcinoma (2–5%) with pulmonary or CNS metastases. Trophoblastic pulmonary emboli may also be seen. Affect 3% of all live births. Since 1980, there has been a 65% ↑ in the frequency of dizygotic (fraternal) twins and a 500% ↑ in triplet and high-order births (most due to the advent of assisted reproductive technology). The incidence of monozygotic (identical) twins has remained steady.


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First_Aid_Step2. Hx/PE: Characterized by rapid uterine growth, excessive maternal weight gain, and palpation of three or more large fetal parts on Leopold’s maneuvers. Dx: Ultrasound; hCG, HPL, and MSAFP are elevated for GA. Tx: Multifetal reduction and selective fetal termination is an option for higher-order multiple pregnancies; antepartum fetal surveillance for IUGR. Management by a high-risk specialist is recommended. Cx: Maternal: Patients are six times more likely to be hospitalized with complications—e.g., preeclampsia, preterm labor, preterm PROM (PPROM), placental abruption, pyelonephritis, and postpartum hemorrhage. Fetal: Complications include twin-to-twin transfusion syndrome, IUGR, and preterm labor. Affects 0.6–1.4% of all deliveries in the United States. Risk factors include obesity, diabetes, a history of a macrosomic infant, and a history of prior shoulder dystocia.


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First_Aid_Step2. Affects 0.6–1.4% of all deliveries in the United States. Risk factors include obesity, diabetes, a history of a macrosomic infant, and a history of prior shoulder dystocia. Diagnosed by a prolonged second stage of labor, recoil of the perineum (“turtle sign”), and lack of spontaneous restitution. In the event of dystocia, be the mother’s HELPER: Help reposition. Episiotomy. Leg elevated (McRoberts’ maneuver). Pressure (suprapubic). Enter the vagina and attempt rotation (Wood’s screw). Reach for the fetal arm. Failure to Progress Associated with chorioamnionitis, occiput posterior position, nulliparity, and elevated birth weight. First-stage protraction or arrest: Labor that fails to produce adequate rates of progressive cervical change. Prolonged second-stage arrest: Nulliparous: Inadequate cervical dilation after > 3 hours with regional anesthesia; > 2 hours without. Multiparous: Inadequate cervical dilation after > 2 hours with regional anesthesia; > 1 hour without.


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First_Aid_Step2. Multiparous: Inadequate cervical dilation after > 2 hours with regional anesthesia; > 1 hour without. See Table 2.11-16. Chorioamnionitis leads to fetal infection, pneumonia, and bacteremia. Some 10% of those affected have permanent injury, 11% have a risk of postpartum hemorrhage, and 3.8% are at risk of fourth-degree laceration. Rupture of Membranes (ROM) Distinguished as follows: Spontaneous ROM: Occurs > 1 hour before onset of labor. May be precipitated by vaginal or cervical infections, abnormal membrane physiology, or cervical incompetence. PPROM: Rupture of membranes occurring at < 37 weeks’ gestation. Prolonged ROM: Defned as rupture > 18 hours prior to delivery. Risk factors include low socioeconomic status (SES), young maternal age, smoking, and STDs. Patients often report a “gush” of clear or blood-tinged amniotic ﬂ uid. Uterine contractions may be present. TABLE 2.11-16. Failure to Progress


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First_Aid_Step2. Patients often report a “gush” of clear or blood-tinged amniotic ﬂ uid. Uterine contractions may be present. TABLE 2.11-16. Failure to Progress First Latent Active Failure to have progressive cervical change: ■Prima: > 20 hours ■Multi: > 14 hours ■Prima: > 2 hrs ■Multi: > 2 hrs after reaching 3–4 cm Second Arrest of fetal descent: ■Prima: > 2 hrs; > 3 hours with epidural ■Multi: > 1 hr; > 2 hrs with epidural Close observation with ↓ in epidural rate and continued oxytocin. Assisted vaginal delivery (forceps or vacuum). C-section. Therapeutic rest via parenteral analgesia; oxytocin; amniotomy; cervical ripening. Amniotomy; oxytocin; C-section if the previous interventions are ineffective. a Augmentation with oxytocin should be considered when contraction frequency is < 3 in a 10-minute period or intensity of contraction is < 25 mmHg above baseline. To minimize the risk of infection, do not perform digital vaginal exams on women with PROM.


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First_Aid_Step2. To minimize the risk of infection, do not perform digital vaginal exams on women with PROM. Preterm labor = regular uterine contractions + concurrent cervical change at < 37 weeks’ gestation. First step: A sterile speculum exam reveals pooling of amniotic fuid in the vaginal vault. Nitrazine paper test is (paper turns blue, indicating alkaline pH of amniotic f uid). Fern test is (a ferning pattern is seen under a microscope after amniotic fuid dries on a glass slide). Second step: Ultrasound to assess amniotic f uid volume. If unsure: Ultrasound-guided transabdominal instillation of indigo carmine dye to check for leakage (unequivocal test). Minimize infection risk; do not perform digital vaginal exams on women who are not in labor or for whom labor is not planned immediately. Check fetal heart tracing, maternal temperature, WBC count, and uterine tenderness for evidence of chorioamnionitis. Depends on GA and fetal lung maturity.


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First_Aid_Step2. Check fetal heart tracing, maternal temperature, WBC count, and uterine tenderness for evidence of chorioamnionitis. Depends on GA and fetal lung maturity. Term: First check GBS status and fetal presentation; then labor may be induced or the patient can be observed for 24–72 hours. > 34–36 weeks’ gestation: Labor induction may be considered. < 32 weeks’ gestation: Expectant management with bed rest and pelvic rest. Antibiotics: Given to prevent infection and to prolong the latency period in the absence of infection. Antenatal corticosteroids (e.g., betamethasone or dexamethasone × 48 hours): Can be given to promote fetal lung maturity in the absence of intra-amniotic infection prior to 32 weeks’ GA. If signs of infection or fetal distress develop, give antibiotics (ampicillin and gentamicin) and induce labor. Preterm labor and delivery, chorioamnionitis, placental abruption, cord prolapse. Defned as onset of labor between 20 and 37 weeks’ gestation.


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First_Aid_Step2. Preterm labor and delivery, chorioamnionitis, placental abruption, cord prolapse. Defned as onset of labor between 20 and 37 weeks’ gestation. Occurs in > 10% of all U.S. pregnancies and is the 1° cause of neonatal morbidity and mortality. Risk factors include multiple gestation, infection, PROM, uterine anomalies, previous preterm labor or delivery, polyhydramnios, placental abruption, poor maternal nutrition, and low SES. Most patients have no identifiable risk factors. Patients may have menstrual-like cramps, onset of low back pain, pelvic pressure, and new vaginal discharge or bleeding. ■ Requires regular uterine contractions (≥ 3 contractions of 30 seconds each over a 30-minute period) and concurrent cervical change at < 37 weeks’ gestation. Assess for contraindications to tocolysis (e.g., infection, nonreassuring fetal testing, placental abruption). Perform a sterile speculum exam to rule out PROM.


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First_Aid_Step2. Assess for contraindications to tocolysis (e.g., infection, nonreassuring fetal testing, placental abruption). Perform a sterile speculum exam to rule out PROM. Obtain an ultrasound to rule out fetal or uterine anomalies, verify GA, and assess fetal presentation and amniotic f uid volume. Obtain cultures for chlamydia, gonorrhea, and GBS. Obtain a UA and urine culture. Hydration and bed rest. Unless contraindicated, begin tocolytic therapy (β-mimetics, MgSO4, CCBs, PGIs) and give steroids to accelerate fetal lung maturation. Give penicillin or ampicillin for GBS prophylaxis if preterm delivery is likely. RDS, intraventricular hemorrhage, PDA, necrotizing enterocolitis, retinopathy of prematurity, bronchopulmonary dysplasia, death.


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First_Aid_Step2. RDS, intraventricular hemorrhage, PDA, necrotizing enterocolitis, retinopathy of prematurity, bronchopulmonary dysplasia, death. Defned as any presentation other than vertex (i.e., head closest to birth canal, chin to chest, occiput anterior). Risk factors include prematurity, prior breech delivery, uterine anomalies, polyor oligohydramnios, multiple gestations, PPROM, hydrocephalus, anencephaly, and placenta previa. Breech presentations are the most common form (affect 3% of all deliveries) and involve presentation of the fetal lower extremities or buttocks into the maternal pelvis (see Figure 2.11-11). Subtypes include the following: Frank breech (50–75%): The thighs are fexed and the knees are extended. Footling breech (20%): One or both legs are extended below the buttocks. Complete breech (5–10%): The thighs and knees are f exed. Follow: Up to 75% spontaneously change to vertex by week 38.


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First_Aid_Step2. Footling breech (20%): One or both legs are extended below the buttocks. Complete breech (5–10%): The thighs and knees are f exed. Follow: Up to 75% spontaneously change to vertex by week 38. External version: If the fetus has not reverted spontaneously, a version may be attempted by applying directed pressure to the maternal abdomen to turn the infant to vertex. The success rate is roughly 50%. Risks of version are placental abruption and cord compression, so be prepared for an emergency C-section if needed. Trial of breech vaginal delivery: Attempt only if delivery is imminent; otherwise contraindicated. Complications include cord prolapse and/or head entrapment. Elective C-section: Recommended given the lower risk of fetal morbidity. Breech presentation is the most common fetal malpresentation. See Table 2.11-17 for indications. For both elective and indicated cesarean delivery, sodium citrate should be used to ↓ gastric acidity and prevent acid aspiration syndrome.


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First_Aid_Step2. See Table 2.11-17 for indications. For both elective and indicated cesarean delivery, sodium citrate should be used to ↓ gastric acidity and prevent acid aspiration syndrome. FIGURE 2.11-11. Types of breech presentations. (Reproduced, with permission, from DeCherney AH. Current Obstetric & Gynecologic Diagnosis & Treatment, 8th ed. Stamford, CT: Appleton & Lange, 1994: 411.) TABLE 2.11-17. Indications for Cesarean Section Surgical extension of the vaginal opening into the perineum. There are two types: median (midline) and mediolateral. Complications include extension to the anal sphincter (third degree) or rectum (fourth degree), which is more common with midline episiotomy, as well as bleeding, infection, dyspareunia, and, in rare cases, rectovaginal fstula formation or maternal death. Routine use of episiotomy is not recommended.


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First_Aid_Step2. Routine use of episiotomy is not recommended. Defned as a loss of > 500 mL of blood for vaginal delivery or > 1000 mL for C-section occurring before, during, or after delivery of the placenta. Table 2.11-18 summarizes common causes. Complications include acute blood loss (potentially fatal), anemia due to chronic blood loss (predisposes to puerperal infection), and Sheehan’s syndrome (pituitary ischemia and necrosis; the 1° cause of anterior pituitary insuffciency in adult females, most commonly presenting as failure to lactate). T AB LE 2.1 1 -1 8. Common Causes of Postpartum Hemorrhage


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First_Aid_Step2. Risk factors Uterine overdistention (multiple gestation, macrosomia, polyhydramnios). Exhausted myometrium (rapid or prolonged labor, oxytocin stimulation). Uterine infection. Conditions interfering with contractions (anesthesia, myomas, MgSO4). Precipitous labor. Operative vaginal delivery (forceps, vacuum extraction). Large infant. Inadequate episiotomy repair. Placenta accreta/increta/percreta. Placenta previa. Uterine leiomyomas. Preterm delivery. Previous C-section/ curettage. Diagnosis Palpation of a soft, enlarged, “boggy” uterus. The most common cause of postpartum hemorrhage (90%). Manual and visual inspection of the lower genital tract for any laceration > 2 cm long. Manual and visual inspection of the placenta and uterine cavity for missing cotyledons. Ultrasound may also be used to inspect the uterus. Treatmenta Bimanual uterine massage (usually successful). Oxytocin infusion. Methergine (methylergonovine) if not hypertensive. Prostaglandin (PGF2a). Surgical repair of the


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First_Aid_Step2. to inspect the uterus. Treatmenta Bimanual uterine massage (usually successful). Oxytocin infusion. Methergine (methylergonovine) if not hypertensive. Prostaglandin (PGF2a). Surgical repair of the physical defect. Manual removal of remaining placental tissue. Curettage with suctioning (take care not to perforate the uterine fundus). a For all uterine causes, when bleeding persists after conventional therapy, uterine/internal iliac artery ligation or hysterectomy can be lifesaving.


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First_Aid_Step2. Postpartum endometritis: The 7 W’s of postpartum fever (10 days postdelivery): Womb (endomyometritis) Wind (atelectasis, pneumonia) Water (UTI) Walk (DVT, pulmonary embolism) Wound (incision, episiotomy) Weaning (breast engorgement, abscess, mastitis) Breastfeeding is contraindicated in maternal HIV infection, active hepatitis, and use of certain medications. Characterized by a temperature ≥ 38°C for at least two of the first ten postpartum days (not including the first 24 hours). Risk factors for postpartum endometritis include emergent C-section, PROM, prolonged labor, multiple intrapartum vaginal exams, intrauterine manipulations, delivery, low SES, young age, prolonged ruptured membranes, bacterial colonization, and corticosteroid use. For endometritis, hospitalize and give broad-spectrum empiric IV antibiotics (e.g., clindamycin and gentamicin) until patients have been afebrile for 48 hours (24 hours for chorioamnionitis). Add ampicillin for complicated cases.


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First_Aid_Step2. For persistent postpartum fever that is not responsive to broad-spectrum antibiotics, think septic pelvic thrombophlebitis, in which pelvic infection leads to infection of the vein wall and intimal damage, leading in turn to thrombogenesis. The clot is then invaded by microorganisms. Suppuration follows, with liquefaction, fragmentation, and, finally, septic embolization. Presents with abdominal and back pain and a picket-fence fever curve (“hectic” fevers) with wide swings from normal to as high as 41°C (105.8°F). Diagnose with blood cultures and CT looking for a pelvic abscess. Treat with broad-spectrum antibiotics and anticoagulation with heparin × 7–10 days. Defned as pituitary ischemia and necrosis that leads to anterior pituitary insuffciency 2° to massive obstetric hemorrhage and shock. Hx/PE: The 1° cause of anterior pituitary insuffciency in adult females. The most common presenting syndrome is failure to lactate (due to ↓ prolactin levels).