Ayesha Hasan, MD, FACC

• Medical Director, Cardiac Transplant Program
• Director, Heart Failure Devices Clinic
• The Ohio State University

Nerve fibers associated with cerebral vessels have been identified mainly within the macrocirculation [42] antibiotic drops for pink eye cheap doxycycline american express, although innervation of the microcirculation has also been suggested [42] xone antibiotic purchase doxycycline in india. There are two proposed origins of these nerves: intrinsic and extrinsic to the brain [2] antibiotic in food discount 100mg doxycycline with mastercard. The extrinsic system arises extracerebrally and consists of sympathetic and parasympathetic autonomic fibers (particularly those arising from the trigeminal system) antibiotics for acne before and after cheap doxycycline 200mg visa, which are found to terminate in the vicinity of large and small conductance vessels with innervation sparse in the pial arterioles (<50 mm) and absent in penetrating arterioles [43] infection 7 weeks after abortion discount 100 mg doxycycline free shipping. Sympathectomized animals have a higher frequency of intracerebral hemorrhage and it was hypothesized that sympathetically induced vasoconstriction protected the brain from intracerebral bleeding during hypertension [48] antibiotics for acne that won't affect birth control order 100mg doxycycline with visa. It is possible that remodeling of large feeding arteries interferes with the normal sympathetic and parasympathetic mechanisms. This hypothesis is presently the most widely accepted and has the most supportive data. With neuronal activation caused by sciatic nerve stimulation, pial arteriolar vasodilatation is observed within 1. The myogenic hypothesis envisions that vascular tone is preset and reflects a balance between the intraluminal and abluminal pressure. Bayliss in 1902 reported direct contraction and relaxation of canine hind limb arteries in response to an increase or decrease of intravascular pressure, respectively, a reaction attributed to intrinsic properties of vascular smooth muscle [55]. In vitro penetrating cerebral arterioles and the steady-state changes in diameter of intracerebral arterioles with changes in intraluminal pressure. Note that with increasing pressure, the arterioles (average diameter 45 m) constrict. With a decrease in intraluminal pressure and possibly flow, the endothelium presumably acts as a mechanoreceptor, transducing variations in transmural pressure and shear stress into altered vascular tone. As will be discussed below, the parenchyma may also participate in the vascular response. Intraluminal hypotension results in vasodilatation whereas intraluminal hypertension results in vasoconstriction. In humans without a history of hypertension, the lower and upper limit of autoregulation is usually stated to be 60­70 mmHg and 130­140 mmHg, respectively, whereas in patients with chronic hypertension, the curve is shifted to the right. As a consequence, increased pressure is transmitted across the capillary network into the precapillary arterioles. However, in vivo animal studies have demonstrated precisely the opposite: increased venous pressure results in pial arteriolar dilatation, as shown in both cats [58] and monkeys [24]. Subsequently, Wei and Kontos [59] elevated venous pressure and, using a closed cranial window, observed pial arterioles in the presence of cerebrospinal fluid containing oxygen-enriched fluorocarbons. In the presence of high oxygen (but not with normal oxygen levels), the vasodilatation induced by elevated venous pressure was converted to vasoconstriction. This observation with oxygen-enriched fluorocarbons indicates that venous hypertension results in cortical hypoxia and/or ischemia of a degree sufficient to cause the release of a metabolic factor from the parenchyma to counteract the myogenic response induced by the venous hypertension. Early studies reached varying conclusions because of the limitations and diversity of investigative methods. With time, instrumentation has improved and methodological limitations were recognized. Nevertheless, even now, most reports involve a limited number of patients, which restricts their statistical power, randomized evaluations are lacking, and blinded analysis rare [61]. Bias is thus the norm and definitive conclusions about hemodynamic factors must be considered with caution. Because of their prolonged exposure to low pressure, the dilated arterioles would be unable to contract ("vasomotor paralysis") and this would expose the remaining microcirculation (capillaries and venules) to unregulated high pressure and flow. Postoperative brain edema and hemorrhage could, therefore, ensue in a small number of patients. An inconsistent temporal component of the hemodynamic and physiological changes may not be recognized, leading to clouding of the data [66]. Despite the limitations of studies noted above, there is considerable support for aspects of this hypothesis [11] based on both patient and laboratory studies. For example, arterioles do not appear to be maximally dilated [67] and they are capable of constricting and dilating; they are not in a state of vasomotor paralysis [30,50,54,67­70]. What is clear is that the hypothesis has fulfilled one of the main purposes, in general, of hypothesis creation: to stimulate interest and hypothesis-testing studies. For example, following experimental head injury [40], there is vasomotor paralysis in both the micro- and macrocirculation. However, the arterioles are able to vasodilate within minutes whereas the larger arteries remain unresponsive for 8­12 hours. This may be correct, but it may not recognize the dynamic changes that have produced the "normal" conditions. Arterial macrocirculation the degree and extent of arterial dilatation may increase with time [11]. There is substantial support for the correlation between small size of the nidus and increased risk of hemorrhage [75­78], although Norris et al. In contrast, transit time through the nidus had no relationship with clinical presentation [61]. Perhaps, the deep locations are less likely to come to medical attention except with hemorrhage, since others investigations have not substantiated the relationship between location and hemorrhage risk [72]. Some studies have found a correlation between artery length and increased risk of hemorrhage [75,81]. Similar to the arterial macrocirculation, the extent and degree of venous dilatation can increase with time. Aneurysms, stenosis, occlusion, and/or vessel wall irregularity have been suggested as being correlated with risk of hemorrhage [18,90]. The degree of venous hypertension will depend on the size of the shunt, the capacitance of the venous drainage in general, and the vagaries specific to individual venous systems [33]. Early studies based on contrast angiography revealed a paucity or delayed filling of perinidal arteries and tissue. The existence of steal has been demonstrated in many [92,94,95], but not all [74,89,96], studies. Some of the disparity may be related to low spatial resolution or to inclusion of patients partially treated by embolization, which can change local hemodynamics and obscure or attenuate the degree of steal [74]. Correlation between hemorrhage and arteriovenous malformations location, venous drainage, and history based on data from 622 untreated patients. Hypoperfusion may not be uniform [98], which has the potential to complicate attempts to correlate hypoperfusion with the size of the shunt. This lack of uniformity may simply be a byproduct of the limitations of the methodology. To some extent, this disparity may reflect technical limitations, different techniques, and/or the parameters analyzed. In addition, brain metabolism will be influenced by whether the patient is studied in the awake or anesthetized state. The underlying mechanisms for such changes are unclear, but they could be related to a primary neural mechanism of reciprocal innervation through transcallosal and intrahemispheric connections. This is increased, perhaps as a reaction to hypoperfusion and to maintain oxygen availability [100]. As already noted, capillary density may be increased to maintain oxygen availability [100]. Elevated venous pressure delays microcirculatory transit time and potentially alters material transfer (including oxygen exchange). However, cerebral edema is rarely observed and the blood­brain barrier is usually intact in the patient pretreatment. Capillaries become pathologically enlarged, which increases their surface area and may affect transfer processes (diffusion and ultrafiltration) unique to the microcirculation [41]. The mechanism for residual vasomotor reserve may be related to the competing influences of low arterial pressure (evoking vasodilatation) and high venous pressure (evoking vasoconstriction) and/or influence of metabolic factors. In the laboratory, low perfusion pressure even within the autoregulatory range [103,104] causes an increase in brain adenosine (a potent vasodilator). Furthermore, pressure autoregulation is impaired by adenosine receptor antagonists (theophylline) and in adenosine receptor knock-out animals [60]. Red cerebral veins: a report on arteriovenous shunts in tumors and cerebral scars. Mechanoreception by the endothelium: mediators and mechanisms of pressureand flow-induced vascular responses. Relationship of nidal vessel radius and wall thickness to brain arteriovenous malformation hemorrhage. Predictors of hemorrhage in patients with untreated brain arteriovenous malformation. Ruptured supratentorial arteriovenous malformations associated with venous aneurysms. Appraising the plasticity of the circle of Willis: a model of hemodynamic modulation in cerebral arteriovenous malformation. The relation of cerebral ischemia, hypoxia, and hypercarbia to the Cushing response. Abnormal balance in the angiopoietin-tie2 system in human brain arteriovenous malformations. The effects of primary elevation of cerebral venous pressure on cerebral hemodynamics and intracranial pressure. The effect of temperature on cerebrovascular resistance and cerebral metabolism in the primate. A radiologic study of the brain circulation by rapid serial angiography of the carotid artery. Haemodynamic evaluation of cerebral arteriovenous malformations by quantification of transit time using high speed digital subtraction angiography: basic considerations. Distributions of local oxygen saturation and its response to changes of mean arterial blood pressure in the cerebral cortex adjacent to arteriovenous malformations. Comparison of the open skull and cranial window preparations in the study of the cerebral microcirculation. Responses of cerebral arteries and arterioles to acute hypotension and hypertension. Blood flow velocity in the pial arteries of cats, with particular reference to the vessel diameter. Adaptation of cerebral circulation to brain arteriovenous malformations increases feeding artery pressure and decreases regional hypotension. Intracranial venous hypertension and the effects of venous outflow obstruction in a rat model of arteriovenous fistula. A new rat model of chronic cerebral hypoperfusion associated with arteriovenous malformations. A model of the pathophysiology of cerebral arteriovenous malformations by a carotid-jugular fistula in the rat. Evidence for adaptive autoregulatory displacement in hypotensive cortical territories adjacent to arteriovenous malformations. Cerebral blood flow response in adenosine 2a receptor knockout mice during transient hypoxic hypoxia. Superselective intraarterial papaverine administration: effect on regional cerebral blood flow in patients with arteriovenous malformations. Cytochrome P450 metabolites of arachidonic acid as intracellular signaling molecules in vascular tissue. Increased venous pressure causes myogenic constriction of cerebral arterioles during local hyperoxia. Role of adenosine A2 receptors in regulation of cerebral blood flow during induced hypotension. A simple relationship between radiological arteriovenous malformation hemodynamics and clinical presentation: a prospective, blinded analysis of 31 cases. Territorial and microvascular perfusion impairment in brain arteriovenous malformations. The use of acetazolamide-enhanced regional cerebral blood flow measurement to predict risk to arteriovenous malformation patients. Changes in cerebral blood oxygenation and hemodynamics after endovascular treatment of vascular malformation measured by time-resolved spectroscopy. Cerebral hyperemia after arteriovenous malformation resection is related to "breakthrough" complications but not to feeding artery pressure. Estimation of shear and flow rates in pial arterioles during somatosensory stimulation. Astrocytes are a key conduit for upstream signaling of vasodilation during cerebral cortical neuronal activation in vivo. Recovery of impaired endotheliumdependent relaxation after fluidpercussion brain injury in cats. Microvascular pathological features of immediate perinidal parenchyma in cerebral arteriovenous malformations: giant bed capillaries. Astroglial and vascular interactions of noradrenaline terminals in the rat cerebral cortex. Lack of sympathetic and cholinergic influences on cerebral vasodilation caused by sciatic nerve stimulation in the rat. Cerebral vasodilatation induced by stimulation of the pterygopalatine ganglion and greater petrosal nerve in anesthetized monkeys. The effect of arteriovenous malformations on the distribution of intracerebral arterial pressures. Simultaneous measurements of pial arteriolar diameter and laser-Doppler flow during somatosensory stimulation. The effect of arteriovenous malformation resection on cerebrovascular reactivity to carbon dioxide. Correlation between intravascular pressure and risk of hemorrhage due to arteriovenous malformations.

Despite this antibiotics in agriculture generic doxycycline 200mg amex, warts are a frequent reason for office visits and dermatology referrals triple antibiotic ointment purchase doxycycline 200 mg amex. The majority of warts can be successfully treated in the primary care setting or even by the patient at home antibiotic home remedies purchase doxycycline 100mg with visa. The plan of care should be based on the clinical appearance antibiotic joint penetration purchase genuine doxycycline, location antibiotics gel for acne order doxycycline 200 mg free shipping, age antibiotics bad for you order doxycycline on line amex, and the immune status of the patient. Treatment is indicated if the lesions are painful or interfere with function, and should be pursued before they multiply and while they are still small. Viruses cannot be seen, so even if the treated area appears normal, the virus may exist in the remaining tissues, and the wart may recur. Current therapies are not wart specific, and the mechanisms of action in existing therapies are either destructive or immunebased. Therapies available are both over-the-counter and in-office treatment; both may take several weeks or months and recurrence is common. A Cochrane review of evidence-based studies showed that salicylic acid and cryotherapy are the two preferred treatment methods. Skin tags are soft, fleshy, pedunculated skin-colored papules that can have a clinical appearance similar to filiform wart, but will lack the characteristic finger-like projections on close examination. A corn or clavus can commonly be mistaken for a wart because of its tendency to interrupt normal skin lines, but will not have the capillary dots when pared. It should be avoided in patients with peripheral neuropathy as the extent of tissue damage can go unnoticed and the risk for impaired healing may exist. These are used in children and on thinner warts in adults, allowing for easy application to multiple areas. However, lower-strength preparations may not be as effective in the treatment of thick or plantar warts. In these cases, more potent preparations containing 40% salicylic acid in plaster form (Mediplast or Duofilm patch) may be used. Cryotherapy, using liquid nitrogen, is the most common in-office treatment of warts. This is useful in older children and adults, but poorly tolerated in young children because of the associated discomfort. Patients should also be instructed to use salicylic acid between treatments after the blister has resolved to aid in resolution. Duct tape is a commonly used household remedy for warts; however, there is conflicting evidence to support its effectiveness. If desired, the silver brand of duct tape that is sticky enough to adhere to the skin is recommended. The goal is to keep the wart occluded with the duct tape as much of the time as possible and can be used in combination with salicylic acid for enhanced benefit. Also known as cantharone, cantharidin is an extract of a blistering insect that is an effective treatment approach for children since the application process is pain-free. The patient can, however, develop pain when the treated sites evolve into blisters. This is a good choice for patients with multiple, thick plantar warts where deeper penetration is needed. Immune-based therapies There have been reports of the off-label use of oral cimetidine given in doses of 30 to 40 mg/kg/day being effective in the treatment of warts. Although this medication is available over the counter, caution should be used when recommending this treatment as there are multiple potential drug interactions associated with its use. Additional immune-based therapies, including topical agents and intralesional treatments, may be available for use by an experienced practitioner in a specialty setting. Advanced treatments or third-line therapies are available, but should be administered by an experienced dermatology provider. Other topical therapies are used effectively but are off label for use in the treatment of warts and include imiquimod cream, 5-fluorouracil, and squaric acid dibutylester. Surgical excision, ablative laser, curettage and desiccation, and snip or shave excision can be performed depending on patient circumstances and office setting. Some dermatology specialists use intralesional immunotherapy with candida antigen or bleomycin. These more aggressive therapies can have significantly higher risks for infection, scarring, and side effects, which should be discussed prior to the procedure with the patient. For patients who do not respond to first- or second-line therapies, consider a referral to a dermatologist for more advanced treatment options. In general, warts of all types are more common and more difficult to treat in immunosuppressed patients. The clinical presentation may be different, making correct diagnosis of the lesion challenging. Pediatrics: Treatment should be aimed at using the least painful methods and lowest potential for permanent side effects like scarring and dyschromia. More destructive methods should be reserved for the most difficult cases where scarring is not a consideration. Pregnancy: Salicylic acid is a pregnancy category C medication and should not be used in pregnant patients due to the possibility of premature closure of the ductus arteriosus associated with its use. Swimming or bathing with an infected person can increase the risk of transmission. It may also be spread by autoinoculation, sexual contact, shared clothing, and towels. Prognosis and Complications Warts are self-limiting and will spontaneously resolve, most within 2 years. Warts that have been present for an extended period of time are less likely to resolve spontaneously. Emphasis should be placed on the fact that warts may take weeks to months to resolve, so that patients do not become discouraged and stop treating lesions at home prematurely. In children, the distribution may be generalized and can range from a few to more than 100 lesions. Genital lesions can occur in up to 10% of childhood cases with widespread involvement. If the genitals are the only area affected, the possibility of sexual abuse should be considered. Mucosal involvement is very uncommon; however, sexually transmitted lesions will occur in the anogenital region or pubis. Molluscum dermatitis, a common phenomenon, is characterized by the Patient Education and Follow-up Education is particularly important for patients treating lesions at home. It is important to review with the patient that salicylic acid will destroy healthy skin as well as the wart, and that the medication should only be applied to the affected area and a few millimeters of surrounding skin to ensure complete treatment. Plain petrolatum can be applied to the normal skin surrounding the wart prior to treatment in order to prevent damage to normal skin. Prior to treatment, it is also helpful to soak the area in warm water to help soften the skin and allow for better penetration of the medication. The patch is then removed, the wart pared down with a nail file or pumice stone, and the process is repeated until the wart has resolved. It is important to instruct patients to follow these steps before reapplying the salicylic acid. It should be noted that whatever tool they are using at home to pare down the warts should be dedicated only for this purpose and should not be used elsewhere on the body, or by other members of the household to minimize autoinoculation or spreading of warts. Instruct the patient to use an electric shaver (not a razor) on warts in hair-bearing areas such as the face or legs. For plantar warts, avoid going barefoot through the house and disinfect the shower base with a diluted bleach solution after bathing. Follow-up is individualized and depends on the patient, the extent of the disease, and the treatment being utilized. If a wart is being treated by the practitioner within the office setting, reasonable follow-up is every 2 to 4 weeks. This challenging skin eruption can have tremendous psychosocial impact that drives patients to seek treatment for the infection. Treatment may be provided in order to prevent lesions from spreading to other areas on the body or transmission to others. All sexually transmitted lesions should be treated along with screening for other sexually transmitted infections. Further treatment indications include pruritus, secondary infection, surrounding dermatitis, or scarring. In cases where there is associated dermatitis or pruritus, the provider may consider treating the patient with a topical agent that will help to repair and maintain the epidermal barrier. There are many additional treatment options available; however, a 2012 Cochrane review concluded that there is no evidence showing that one method is convincingly more effective than the others. Topical treatment is common and includes the use of cantharidin, Diagnostics Diagnosis is clinically made by the characteristic appearance of the lesions. Solitary lesions or a giant molluscum that occurs on the face can be differentiated from basal cell carcinomas that typically present as a translucent skin-colored papule with telangiectasias and rolled borders. Biopsy is not necessary but may be performed to confirm the diagnosis especially in the case of large lesions or extensive involvement. The virus itself cannot be cultured; however, bacterial culture may be needed if there is concern for secondary infection. If the central umbilication or dell is not obvious, a dermatoscope or magnifying lens may help identify the central core. The contents from the central core contain most of the viral cells and can be directly examined with microscopy. Normal epithelial cells are flat, varied rectangular shapes, and tend to remain stuck together in sheets. Lightly spraying or touching the surface of the lesion with liquid nitrogen will often reveal this distinctive finding. ChaPter 10 · viral iNfectioNs as discussed previously in the treatment of verruca. Since the application is painless, children are more cooperative, but painful blisters may follow application. Clinicians should consider testing 2 to 3 lesions initially to ensure that the patient does not have sensitivity to it. Cryotherapy is a destructive method that can be used in primary care but has limitations due to the discomfort of the procedure, especially in children. Curettage is a successful method used by experienced clinicians for treatment in children or adults with a limited number of lesions. This method may also cause a small scar so the treatment site should be chosen carefully. Less invasive approaches include application of surgical or duct tape daily (after bathing) for 16 weeks, which can lead to a cure in up to 90% of children. Patients with atopic dermatitis and a history of molluscum and/or flat warts can benefit from regular moisturizing with a preparation containing ceramides to protect the normal skin barrier and help prevent autoinoculation. Treatment modalities that may be utilized in a dermatology setting include imiquimod, podophyllotoxin 0. Lesions located in the periocular region should be referred to an ophthalmologist for management. The virus replicates at the site of inoculation and then travels along the dorsal root ganglion where it becomes dormant until reactivation. When the patient has his/her first clinical lesion, this is usually a recurrence and represents the secondary phase. Various triggers can reactivate the virus and include, but are not limited to , sun exposure, stress, and physical trauma. Genital lesions: Should raise suspicion for other sexually transmitted infections. Pregnancy: Curettage, cryotherapy, and incision with expression of the central core are all safe treatment options to use during pregnancy. Podophyllin, podofilox, and imiquimod are all teratogenic and are contraindicated during pregnancy. These vesicles will then turn into pustules, umbilicate, and subsequently dry and form crusts on the skin, or exudate on mucous membranes. Presentation can vary based on factors such as anatomical location and immunosuppression. Clinical hallmarks of the latter include pain, an active vesicular border, and a scalloped periphery. Early vesicles may never be seen, lesions may appear as erosions or crusts, and presentation is often atypical in this population. Patient Education and Follow-up While it is not necessary to isolate the infected individuals, patients and parents of infected children should be educated on transmissionreducing methods. Lesions in areas that are likely to come in contact with others, such as those on the arms or legs, should be covered with clothing or a watertight bandage. Infected children should not bathe with others, and towels should not be shared in order to prevent spread of infection. This presents as herpetic lesions on the oral mucosa, tongue, and tonsils, accompanied by flu-like symptoms. Patients can be acutely ill, and in severe cases may require treatment with intravenous antiviral therapy. Primary infection is usually associated with more constitutional symptoms, longer duration, and prolonged viral shedding when compared to recurrent episodes. Lesions can also occur wherever the virus was inoculated or proliferated during the initial episode, such as inside the mouth, cheeks, eyelids, or earlobes. Other associated clinical symptoms can include local discomfort, headache, nasal congestion, and mild flu-like symptoms, including fever. Herpes gladiatorum Herpes gladiatorum is the name given to the herpes infection which results from direct skin-to-skin exposure through contact sports. Wrestlers are especially at increased risk, and the condition can be a major problem during school tournaments and sports camps. It has been estimated that up to one third of wrestlers will become infected after a single match with an infected individual.

Polyps found in the stomach and small intestines are likely diagnosed in childhood and young adults infection kidney stones discount 100 mg doxycycline with mastercard. They also have increased risk of breast cancer virus 7912 purchase doxycycline with american express, pancreatic cancer antibiotics for acne alternatives cheap 100mg doxycycline, and reproductive neoplasms when compared to the general population new antibiotics for sinus infection order discount doxycycline on-line. Referral and Consultation Referral to a gastroenterology provider is important for appropriate screening antibiotics given for sinus infection uk discount 100mg doxycycline fast delivery, diagnosis virus 46 purchase doxycycline 100mg overnight delivery, and management. The importance of all cancer screenings and early recognition of disease should be reinforced. Hepatoerythropoietic porphyria, congenital erythropoietic porphyria, and erythropoietic protoporphyria are also nonacute types that are uncommon. Porphyria cutanea tarda is the most common and most readily treated type of porphyria. It is associated with individuals who have hepatic iron overload and liver disease. The result is the release (or activation) of dermal mast cells, leading to skin fragility, vesicles, and bullae. Clinical Presentation Photosensitivity is the most common cutaneous manifestation of nonacute porphyrias. Increased skin fragility and scleroderma-like plaques (indurated and waxy) may be present on the neck, preauricular area, chest, and back. Facial hypertrichosis is a hallmark characteristic that occurs on the zygoma and malar prominences. A chemistry panel with special attention to liver function studies is important to evaluate the patient for liver disease. It is imperative to identify and avoid triggers such as sun exposure, alcohol, and estrogen therapy. Hemoglobin, serum ferritin, and serum or plasma porphyrin levels must be monitored at least quarterly. Regular health maintenance and monitoring for complications including hepatic tumors should be emphasized. It has a higher incidence in children (fair-skinned) compared to adults, and women more than men. Other causative medications include antibiotics (tetracyclines and quinolones), furosemide, amiodarone, dapsone, voriconazole, nabumetone, and oxaprozin. Phlebotomy is the most common treatment used to reduce the iron overload and performed regularly until ferritin levels normalize. Yet patients with pseudoporphyria do not have hypertrichosis, hyperpigmentation, or sclerodermoid changes-important diagnostic clues. However, the skin fragility, blistering, and associated pain make performing certain jobs difficult, if not impossible. Consultation with a dermatology provider for skin evaluation and biopsy may be considered. Phlebotomy and iron chelation therapies may best be managed by a referral to a hematologist. Diagnostics True porphyria must be ruled out in patients suspected of having pseudoporphyria. Patient Education and Follow-up Patients should be educated on the importance of following the prescribed treatment plan and follow-up. Prognosis and Complications the prognosis for pseudoporphyria is good except for possible permanent scarring and abnormal pigmentation from the lesions. Patient Education and Follow-up If pseudoporphyria was drug induced, it is important for the patient to avoid that drug and all others in the drug classification. The patient should be instructed to avoid excessive sun exposure and to avoid tanning beds. Periodic follow-up is helpful to make sure the patient is following the recommended plan of avoidance therapy. Hyperkeratotic papules are present on extensor areas of the upper extremity in a diabetic patient with renal failure and undergoing dialysis. If confirmed, serology should include a basic metabolic panel to assess for diabetes and renal failure. The dermal theory of pathogenesis proposes that the metabolic derangement associated with chronic renal failure and diabetes induce superficial dermal connective tissue changes triggering the transepidermal elimination. Others suggest that it is a primary defect in the epidermis or an abnormal healing response to injury. Management Recognition and treatment of any underlying disease is the first priority. Topical keratolytics such as salicylic acid, lactic acid, or urea may be initiated but should be used cautiously if there is broken skin or erosions. Alternatively, intralesional corticosteroids, systemic retinoids, and cryotherapy have also been reported with mixed response. Clinical Presentation Patients present with umbilicated dome-shaped papules on the arms and legs. A linear configuration suggests a koebnerization (lesions in the location of previous trauma or pressure). Otherwise, the prognosis and complications are based on the underlying disease state. Referral to a dermatologist is usually for diagnosis and management of severe cutaneous symptoms. Patient Education and Follow-up Patients should be educated to avoid scratching, rubbing, and other trauma to the areas. Educating the patient on proper hydration of the skin and use of emollients is helpful. It is associated mainly with individuals with chronic renal failure and secondary hyperparathyroidism. Diagnostics Patients suspected of having calciphylaxis should be referred to a dermatologist immediately. Diagnosis of calciphylaxis requires a deep excisional biopsy to ensure that subcutaneous tissue is submitted for histological analysis. Serum calcium, phosphorus, parathyroid hormone, aluminum, urea nitrogen, creatinine, and albumin are critical. Pathophysiology Accumulation of calcium deposits in the tunica media of the walls of small- and medium-sized vessels results in occlusion and ultimately tissue necrosis. It has been suggested that it may be due to a uremic-induced defect, chronic inflammation, or other processes that impact bone metabolism and calcification. Management A treatment plan for the calciphylaxis patient should begin with ongoing assessment and treatment of renal failure by nephrology. Hyperparathyroidism should be addressed to manage abnormal serum calcium and phosphorus levels. Surgical and wound care specialists may consider hyperbaric oxygen therapy or sodium thiosulfate infusions. Some novel treatments have been employed but require a multidisciplinary team approach from experienced specialists. Clinical Presentation Early presentation of calciphylaxis resembles livedo reticularis with the mottled pattern of cyanosis. There may be one or several lesions that are commonly located on the lower legs, thighs, buttocks, and lower abdomen. Prognosis and Complications Calciphylaxis, especially when it has progressed to ulcerations, has a high mortality rate of 60% to 80%. The 1-year and 5-year survival rates have been reported at 45% and 35%, respectively. Counseling can be important in helping patients and their families deal with this physically and psychologically devastating disease. Patient Education and Follow-up Weekly, and sometimes more often, follow-ups are usually necessary for these patients. Metabolic syndrome is a combination of obesity (especially truncal), elevated blood glucose, hyperlipidemia, and hypertension. It is more common in dark skin tone races, including Native Americans, Hispanics, and African Americans. In these situations, the cause may be related to insulin binding insulin-like growth factor receptors on keratinocytes and dermal fibroblast proliferation. The axillae, groin, umbilicus, areolae, submammary regions, and hands can develop these characteristic lesions. Screening for insulin resistance should include a glycosylated hemoglobin (hemoglobin A1c) and fasting blood sugar, although a normal level does not rule out insulin resistance. Management When obesity is a factor, weight loss can eliminate or improve the lesions. Cosmetic improvement may be achieved with application of topical retinoids, preparations with salicylic acid, ammonium lactate lotion or cream, 20% topical urea, or alpha hydroxyl acids. Endocrinology may be consulted as needed to assist in the diagnosis and management of a possible metabolic disorder. Follow-up should be done to evaluate the efficacy of therapy and to monitor the insulin resistance. Patient education and follow-up Patients should be educated on importance of good glycemic control, proper skin care avoidance of trauma to the affected areas. Diabetic Bullae Diabetic bullae or bullosis diabeticorum develop in approximately 0. Pathophysiology the pathogenesis of diabetic bullae is poorly understood and is likely multifactorial. Evidence also suggests an abnormality of anchoring fibrils that are essential for the integrity of the dermoepidermal junction. The threshold for suction related blister formation is lower for diabetics than nondiabetics. Clinical presentation these bullae appear suddenly and favor acral skin areas, especially the dorsal and lateral aspects of the lower legs and feet. If considered, the benefit of biopsy must be weighed against the risk of slow healing, infection, and ulceration on the lower extremities of a diabetic patient. There are a wide variety of skin changes and disorders that are associated or caused by dysregulation of the thyroid gland. Correcting the thyroid hormone levels can lead to resolution of the skin conditions. Low levels of circulating thyroid hormone or cell resistance to thyroid hormone action can result in hypothyroidism. The most common cause for hypothyroidism is the autoimmune disease Hashimoto thyroiditis, which results in glandular failure. Hypothyroidism can be genetic, or it may also be the result of surgical procedures and radiation to the head and neck. Hyperthyroidism results when there are excessive levels of circulating thyroid hormones usually due to an autoimmune disease called Graves disease. Hyperthyroidism can also develop due to thyroid adenomas, inflammation of the thyroid, excess iron intake, and in the postpartum period. The skin responds when there are inadequate or excessive amounts of circulating thyroid hormone. There can be a direct or indirect effect on the skin as thyroid dysfunction affects all organs and body systems, thus resulting in cutaneous systems. In a hyperthyroid state, many cutaneous manifestations are due to increased cutaneous blood flow and peripheral vasodilatation. In a hypothyroid state, symptoms may be associated with a reduced core body temperature and reflex cutaneous vasoconstriction. Diagnostics A tissue biopsy for histology and direct immunofluorescence is indicated to exclude other blistering disorders of the skin. Management Since the bullae heal spontaneously, treatment is focused on the avoidance and treatment of secondary infections. Should the blister become unroofed, aggressive wound healing measures should be taken. Referral and consultation Refer diabetic bullae patients to dermatology for appropriate biopsy if needed to rule out other blistering skin disorders. If wounds from unroofed blisters are resistant to healing, refer to dermatology as soon as possible to avoid ulceration and necrosis. Once necrosis occurs the patient may require referral to a surgeon for debridement and skin grafting. Patient education and follow-up Patients with diabetic bullae should be monitored closely until the bullae have healed and resolved. Since the bullae are prone to recur, the patient should be evaluated with each episode. Good skin Clinical Presentation In addition to the skin changes noted in Table 19-3, other cutaneous manifestations may be present from disease or conditions associated with thyroid disease. A free or total T4 should be performed but may be affected by pregnancy, disease states, or genetic predisposition. Management Most of the cutaneous manifestations of thyroid dysfunction are managed by treating the specific thyroid problem. Since thyroid regulation occurs in a slow negative feedback loop, it can take several weeks for the thyroid levels to normalize once appropriate therapy has been instituted. In hyperthyroidism, ablation with radioactive therapy or surgical thyroidectomy is the most common treatment. Prognosis and Complication Prognosis is good for individuals with thyroid dysfunction. Once corrected, symptoms usually resolve but may be dependent on the severity, chronicity, comorbidities, and treatment. Hyperthyroid patients undergoing thyroid ablation should be monitored for hypothyroidism. Half of the patients with Graves disease have ocular symptoms, with about 5% having severe ophthalmopathy. Graves disease requires management by an endocrinologist and often an ophthalmologist.

Horizontal incisions are made on the nasopharyngeal surface of the soft palate and the overlying mucosa is elevated antibiotics history cheap 200 mg doxycycline free shipping. Lateral incisions are created to free the mucosa from the upper surface of the soft palate antibiotic resistant uti doxycycline 200mg line, allowing the mucosal flaps to be reflected posteriorly antibiotics for uti in rabbits purchase doxycycline line. The pharyngeal flap is incorporated into the soft palate closure antibiotic resistance newspaper article cheap 200mg doxycycline with mastercard, high in the nasopharynx antibiotics for resistant sinus infection discount 200 mg doxycycline otc, with horizontal mattress sutures similar to those used for a conventional flap antibiotic resistance lab activity generic doxycycline 200mg online. The mucosal flaps of the soft palate are reflected posteriorly and are sutured to the raw undersurface of the pharyngeal flap. Alternate Palate Splitting Technique for Pharyngeal Flap the harvest of the posterior pharyngeal wall myomucosal flap is the same as detailed previously. Rather than incising the posterior soft palate, the midline of the soft palate is split in a full thickness incision to the midpoint of the soft palate between the tip of the uvula toward the hard palate. With the endotracheal tubes in place on the lateral aspect of the flaps, the myomucosal flap is then inset into the apex of the split in the soft palate. A repeat office evaluation for objective resonance testing occurs 3 months postoperatively. If hypernasality or nasal emission is detected, repeat nasopharyngoscopy is performed. Complications Complications of the pharyngeal flap are generally related to the flap itself. If the flap is too narrow, most commonly a result of scar contracture from secondary intention healing, the lateral velopharyngeal ports are too large and the flap acts as an inappropriately sized obturator. A flap that is set too far inferior may tether the free edge of the soft palate and prevent proper elevation during closure attempts, resulting in incomplete closure and nasal escape. Pharyngeal flaps that are exceptionally wide may obstruct the nasopharynx and lead to hyponasality, and, potentially, obstructive sleep apnea. Continued scar contracture around the lateral ports may cause stenosis of these areas and subsequent airway difficulties. Tylenol is administered for pain control during the first 24 hours, after which ibuprofen is added. Intravenous fluids are given for the duration of the hospital stay and perioperative oral antibiotics (amoxicillin/sulbactam or clindamycin) are continued for 1 week. Nasal stents are irrigated with normal saline and suctioned as necessary; elbow cuffs are used to protect them. The stents are removed the morning after surgery, and the child is discharged after demonstrating an adequate airway and adequate oral intake; this usually occurs 48 hours postoperatively. Steroids are advocated by some surgeons to decrease airway edema and improve postoperative inflammation. To maximize functional use of the pharyngeal flap, speech therapy should also begin at this time and continue as Assessing the Need for Revision Surgery It is important to note that not all patients with continued hypernasality require revision surgery, as developmental delays, compensatory articulation errors, and underlying syndromes can affect speech outcomes. As mentioned 12PharyngealFlapSurgery earlier in this chapter, an objective assessment of surgical outcomes should be obtained after a course of speech therapy. If abnormal resonance or nasal air emission is identified, nasopharyngoscopy should be performed to visualize the adequacy of velopharyngeal closure and determine the etiology of a persistent problem. Surgical repairs should be evaluated for their location within the velopharyngeal sphincter. Ports that are too large cannot be completely closed by medial movement of the lateral pharyngeal walls. Asymmetric lateral wall motion or a flap that is skewed to one side may demonstrate air leakage only on one side of the velopharyngeal sphincter. If airway obstructive symptoms persist beyond 3 months, it is unlikely that improvement will spontaneously develop in the near future. Although continuous positive airway pressure may temporize the problem, the child will remain technology dependent unless a revision procedure is performed. A pharyngeal flap may be redone, and adequate laxity in the surrounding tissue allows a second procedure to be successfully accomplished. Closure of the donor sites may be slightly more difficult, although it is generally not problematic. It also allows anatomic landmarks to be identified, ensuring that the flap is elevated sufficiently to contribute to velopharyngeal closure. Inspection of the velopharyngeal inlet with a mirror after the donor site is closed can ensure this complication will not develop. If it is visible on examination of the oropharynx, it is too low and will not function properly. Care should be taken not to "wrap" the flap around the stents, as stenosis of the ports will develop. Space anterior to the stent will not create a problem with velopharyngeal closure. In some institutions, however, this approach is rivaled by sphincter pharyngoplasty. Despite attempts to determine the clear superiority of one of these two popular approaches, high-level evidence-based studies have not yet been conducted. Nonetheless, prompted by concerns regarding reported complications associated with pharyngeal flaps, Cole et al. These authors concluded that when coupled with a thorough preoperative evaluation, meticulous technique, and close perioperative monitoring, the pharyngeal flap is a safe and reliable surgical option. The repair of cleft palates after unsuccessful operations, with special reference to cases with an extensive loss of palatal tissue. A clarification of the goals in cleft palate speech and the introduction of the lateral port control (L. A review of the evaluation and management of velopharyngeal insufficiency in children. A comparison of speech results after the pharyngeal flap and the dynamic sphincteroplasty procedures. Comparison of speech improvement in cases of cleft palate after two methods of pharyngoplasty. Plast Reconstr Surg Transplant Bull 1962;30:36­42 PubMed 176 Complete Cleft Care 10. Two hundred twenty-two consecutive pharyngeal flaps: an analysis of postoperative complications. J Oral Maxillofac Surg 2008;66(4):745­748 PubMed 13 Sphincter Pharyngoplasty Emily F. In the Furlow double-opposing Z-palatoplasty, the levator veli palatini musculature is reoriented from its aberrant sagittal positioning to a more natural transverse orientation, while opposing oral and nasal flaps are transposed into a "z. The healed sphincter (transposed myomucosal flaps) augments the posterior pharyngeal wall aspect of the velopharynx and approximates the palate upon closure. Sphincter pharyngoplasty is conceptually different from the posterior pharyngeal flap. It involves horizontal transposition of two vertical, lateral, superiorly based pharyngeal myomucosal flaps across the posterior aspect of the velopharynx to create a single central port. As suggested by its name, the goal of sphincter pharyngoplasty is to augment the velopharyngeal sphincter. The benefit from sphincter pharyngoplasty is primarily attributed to augmentation of the posterior pharyngeal wall, as electromyographic studies evaluating dynamic muscular activity of the neo-sphincter have shown no intrinsic muscular activity. In 1950, Hynes described elevation of bilateral superiorly based palatopharyngeus myomucosal flaps, rotated 90 degrees and sutured into a transverse mucosal incision made just inferior to the nasopharyngeal tori. Additionally, he performed the procedure in children who had open soft palatal clefts; when the palate was intact, it was divided to improve nasopharyngeal exposure. Although several variations of this procedure have been proposed, the most notable was by Orticochea in 1968. A speech-language pathologist who is adept at evaluating velopharyngeal function in children should perform a complete speech assessment. Following patient history, physical examination, and thorough speech evaluation, an instrumental assessment is performed. Strengths and limitations of these two procedures are discussed in detail in Chapter 11. Notation is made of gap size in addition to degree of inward motion of the velum and lateral and posterior pharyngeal walls. Coronal pattern of closure ideal for surgical management with sphincter pharyngoplasty. Notably the musculus uvula bulges centrally and posteriorly toward the pharyngeal wall, indicating transverse orientation of the levator veli palatini. The sphincter pharyngoplasty can be tailored by surgeons to suit the velopharyngeal deficit of the individual patient. The Procedure Preoperative Assessment and Planning A thorough preoperative assessment of velopharyngeal function should precede decision for sphincter pharyngoplasty. A thorough patient and family history of cleft deformities should also be obtained, in addition to any history of syndromic abnormalities. View of nasal surface of soft palate on endoscopy showing distinct groove, indicating longitudinal orientation of the levator veli palatini, or submucous cleft palate. Barium drops are instilled into the nasal passage and fluoroscopic images of speech samples are obtained, typically in a total span of 80 to 120 seconds. The presence of a midline groove along the nasal surface of the soft palate can be indicative of sagittal-positioned levator veli palatini muscles and/or the presence of a submucosal cleft palate. Furlow palatoplasty is performed as the primary procedure of choice when a groove is identified and the velopharyngeal gap is, 50%. At this point, a "moment of silence" is performed to evaluate for aberrant or robust palpations that could suggest medialization of the carotid arteries. This observation is made prior to injection of local anesthesia and incision planning. A red rubber catheter is inserted into the nasal cavity and viewed in the oropharynx. Next, a silk suture (2-0) is placed along the oral surface of the base of the uvula and tied to the catheter. The catheter is retracted through the nose so that the uvula and palate are retracted posteriorly and superiorly to allow for exposure of the nasopharynx. Silk sutures may also be placed through the tonsillar pillars in order to provide retraction of the lateral walls and further improve visualization. These incisions are typically drawn posterior and lateral to the posterior tonsillar pillars inferiorly down to the inferior pole of the tonsil. Local anesthesia with vasoconstrictive activity (commonly 1% lidocaine with 1:100,000 epinephrine) is injected into a submucosal plane along the posterior and lateral walls of the velopharynx, including the caudal aspect of the nasopharynx and adenoid pad. Using angled or Metzenbaum scissors, blunt dissection (horizontally directed) is used to identify the alar fascia, which appears as a solid white sheen. Once this plane is identified, sharp dissection (vertically directed) is used to isolate the muscle from the fascia along the length of the flap superiorly and inferiorly. Care is taken to direct the scissors outward from the edge in order to maximize muscle within the flap. Particular care is taken when dissecting muscle superiorly along the lateral aspect of the flap to avoid inadvertent carotid injury. Finally, the inferior aspect of the flap is transected, and a 4-0 absorbable suture is placed through the distal tip of the flap, encompassing both muscle and overlying mucosa. On examination, the oropharynx should be assessed for presence of tonsillar hypertrophy. Children with obstructive symptoms and tonsillar hypertrophy should undergo tonsillectomy as a staged procedure 2 to 3 months prior to planned sphincter pharyngoplasty. We generally plan for repeat nasoendoscopy 6 to 8 weeks after tonsillectomy to reassess the pattern and size of the velopharyngeal gap prior to sphincter pharyngoplasty. The inferior aspects of the donor sites are now closed using simple interrupted 4-0 chromic sutures. Some surgeons may opt to leave the donor sites open to heal by secondary intention. The recipient site is planned 1 to 2 mm inferior to the caudal edge of the adenoid pad. This places the rotated myomucosal flaps above the soft palate when viewed through the oropharynx in normal anatomic position. Preplacement of these sutures is extremely helpful in securing the superior myomucosal flap after it is horizontally transposed, as visualization is significantly easier prior to rotation of the bulky flap. The optimal position of the superior flap is determined by the amount of augmentation required for the particular patient. The preplaced superior mucosal sutures are placed through the midportions of the rotated superior flap and secured, taking care to achieve mucosal approximation. In similar fashion, the contralateral flap is then transposed and secured inferiorly to the superior flap. Interrupted sutures are placed to secure the inferior mucosal edge of the recipient site to the bottom edge of the inferior myomucosal flap. The degree of lateral transposition of this inferior flap will determine the amount of augmentation achieved, where a more lateral placement will create a greater sphincteric effect. For example, the surgeon can adjust the composition of the myomucosal flaps to include the posterior tonsillar pillars, posterior pharyngeal wall musculature, or both, depending on the degree of augmentation required. The dimensions and shape of the flaps, such as length into the oropharynx or medial/lateral width, may also be adjusted. Furthermore, the degree of sphincteric augmentation may be accentuated or minimized with the lateral positioning and degree of overlap of the flaps once they are rotated horizontally into position. The amount of mucosa removed at the recipient bed can be adjusted to compensate for the dimensions of the lateral flaps and amount of augmentation required. Postoperative Care the child is admitted overnight to monitor for airway obstruction and to administer intravenous hydration. Many surgeons prefer a soft diet for 2 to 3 weeks postoperatively to prevent disruption of the neo-sphincter prior to complete healing.

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The vasocorona has perforators that centripetally supply the white matter of the peripheral spinal cord (rami perforantes) [2] antibiotic bronchitis order doxycycline online pills. Segmental arteries the level of each segmental artery corresponds to the spinal level it supplies rather than its site of origin from the aorta bacteria jacuzzi discount doxycycline line. In the upper thoracic spine antibiotic for uti pseudomonas discount doxycycline 200 mg with visa, the segmental arteries can exit the aorta up to two levels caudal to the vertebral levels they supply bacteria and archaea similarities cheap 200 mg doxycycline. The midthoracic segmental arteries generally exit just below their corresponding vertebral levels 2013 200mg doxycycline with mastercard, and the lumbar segmental vessels arise typically at their respective vertebral levels virus check buy doxycycline 200 mg mastercard. Because the aorta is located anterior to the spinal cord, the left segmental arteries generally exit the aorta posteriorly and the right segmental arteries originate medially [3]. The spinal branch enters the intervertebral foramen and splits into (1) the retrocorporeal (anterior spinal canal) and prelaminar (posterior spinal canal) arteries, and (2) a radicular artery. The radicular artery supplies nerve roots and dura at every level as the radiculoradial or radiculomeningeal arteries. At certain levels, the radicular artery supplies the spinal cord via branches known as the radiculomedullary arteries. This vessel descends over the central sulcus of the anterior cord all the way to the conus medullaris [5]. Selective right vertebral artery catheter angiogram (frontal view) demonstrates the artery of cervical enlargement (arrow) supplying the anterior spinal artery (arrowheads). The lower lumbar segmental arteries, specifically at L4 and L5, can originate below the level of the aorta. Selective left vertebral artery catheter angiogram (frontal view) shows the anterior spinal artery (arrowheads) originating from the left vertebral artery (arrow) distal to the posterior inferior cerebellar artery origin. It is worth delineating the course of these arteries from the aorta to the spinal cord. In the thoracic spine, caudally from the T3 level, there are, on average, 10 pairs of segmental arteries exiting from the aorta. Above T3, a supreme intercostal artery emanates from the aorta and can Intrinsic system Venous drainage is not directly analogous to the arterial anatomy. The peripheral, or radial, veins originate in the capillaries at the gray­white junction and are directed centrifugally. The central, or sulcal, veins drain from the medial aspects of both halves of the spinal cord, specifically from the anterior horns, anterior commissure, and the white matter in the anterior funiculus [1]. Extrinsic system Unlike the intrinsic system, it is convenient to correlate the superficial extrinsic venous system with the arterial system. Two lower thoracic selective catheter spinal angiograms (frontal views) depicting the typical "hairpin" turn of the artery of Adamkiewicz (arrow), which supplies the anterior spinal artery (arrowheads). The hemivertebral blush is noted in (A), confirming the midline position of the anterior spinal artery. Posteriorly, there is usually a dominant posterior median vein, but smaller posterolateral veins often accompany this vessel [1]. The anterior and posterior median spinal veins subsequently drain into the anterior and posterior radiculomedullary veins, respectively, which then drain into epidural venous plexi. There are, on average, 8­14 anterior radiculomedullary veins [9] and 5­10 posterior radiculomedullary veins [5]. The venous phase must appear within 10 seconds, otherwise it should be considered an abnormal finding and a spinal dural arteriovenous fistula must be suspected. On average, three tortuous posterior median spinal veins and the anterior median spinal vein descend towards the epidural venous plexus via the posterior and anterior radiculomedullary veins [1]. On axial views, the epidural venous plexi are best represented diagrammatically with the anterior external vertebral venous plexus and basivertebral vein draining the vertebral body and the anterior internal vertebral venous plexus draining the epidural space. When discussing the normal anatomy of the spinal venous system, it is necessary to discuss physiological mechanisms behind the venous drainage in the lower spinal cord. Many theories exist as to how autoregulation of venous pressure occurs in the spinal cord to prevent venous reflux under the umbrella of 32 Chapter 3: Spinal vascular anatomy and implications for treatment the "anti-reflux mechanism. Other structures to explain the anti-reflux mechanism have been discovered that will help to control venous pressure, including intravenous intradural folds, narrowing of radicular veins upon their entrance to the dura, increased smooth muscle fibers in these veins to assist in regulating waves in pressure, and a tortuous course to assist in siphoning increases in venous pressure [12,13]. Embryology Embryologically, bilateral capillary networks on the ventrolateral surface of the cord connect with segmental branches of the aorta. This variable segmental artery regression also leads to the origination of the vertebral arteries, thyrocervical trunks, and costocervical trunks in the cervical region and the iliac arteries in the lumbar region [15]. Venous networks are forming as these arterial anastomoses develop early in the embryo. It is thought that many vascular malformations can originate at this critical time, three to six weeks after gestation [16]. Selective median sacral artery angiogram (frontal view) originating from the aorta (white arrows). Bilateral L5 segmental arteries are seen originating from this vessel (black arrows). Selective catheter spinal angiograms showing the differences between the anterior (A) and posterior (B) radiculomedullary arteries. The extraspinal system, also known as the paravertebral anastomotic network, is a longitudinal network that runs along the lateral aspect of the vertebral bodies and is best defined in the cervical spine where the vertebral artery, ascending cervical artery, and deep cervical arteries can communicate [18]. The intraspinal system, or retrocorporeal arterial network, is primarily a transverse network that connects the right and left segmental arteries and is best recognized as a diamond-shaped network located in the dorsal epidural space posterior to the vertebral bodies [15]. Pial anastomoses the pial arterial network, also known as the vasocorona, is an arterioarterial connection between the anterior and posterior spinal systems that is not visualized on a normal spinal angiogram because of the small caliber of these vessels, although it visible in high-flow lesions such as arteriovenous malformations [15]. Radicular arteries from the cauda equina also go through this network because of the abundant vascular arterial supply [15]. The central­peripheral type connects sulcal and radial veins and the transmedullary type is a midline anastomosis of the left and right median veins [18]. It should be noted that the transmedullary system is largest in the cervicothoracic spine [5]. Although a thorough investigation of all potential spinal anastomoses is needed to diagnose a treatable lesion, occasionally angiography must look beyond the spine itself. One additional pathological anastomosis is the type 5 craniocervical dural arteriovenous fistula, which can clinically present as dysfunction of the upper cord or lower brainstem and radiographically with edema in the cervical spine and/or brainstem. The existence of these fistulae underlines the need not only for a spinal angiogram but also for cerebral angiography when searching for treatable lesions [19­23]. Spinal anastomoses Knowledge of spinal anastomotic networks is essential for an adequate characterization of spinal vascular lesions and subsequent treatment of these abnormalities. Failure to do so may result in inaccurate false-negative spinal angiograms or incompletely treated arteriovenous malformations [17]. Left T11 angiograms with a prolonged injection of contrast to better visualize the angioanatomy at the conus medullaris. Origins of the segmental arteries in the aorta: an anatomical study for selective catheterization with spinal arteriography. Vascular Anatomy of the Spinal Cord: Neuroradiological Investigations and Clinical Syndromes. The angiosome territories of the spinal cord: exploring the issue of preoperative spinal angiography. Anatomical and pathological considerations in percutaneous vertebroplasty and kyphoplasty: a reappraisal of the vertebral venous system. Paravertebral arteriovenous malformations with epidural drainage: clinical spectrum, imaging features, and results of treatment. Practical Neurology: Vascular Anatomy of the Spinal Cord and Spinal Cord Ischaemia. Dural arteriovenous fistulas presenting with brainstem dysfunction: diagnosis and surgical treatment. Classification and endovascular treatment of spinal cord arteriovenous malformations and fistulas. Endovascular treatment of intracranial dural arteriovenous fistulas with spinal perimedullary venous drainage. These malformations are characterized by a direct connection between the arterial and venous systems. This low resistance connection has physiological and pathological consequences on the surrounding and, in some cases, distant nervous tissue. Some of the confusion may stem from the fact that these clinical observations are based on a mature or relative steady-state lesion where the present status has been created by dynamic and reactive physiological and pathological forces. The cerebral circulation can be divided into macro (arteries and veins) and micro (arterioles, capillaries, and venules) components. Macrocirculation Arteries the arterial component of the macrocirculation comprises large conductance vessels whose walls contain vascular smooth muscle [2]. The branching architecture influences the flow pattern with acute angle branches (<30 degrees) receiving more flow than arteries whose branching is less acute (60­90 degrees). In general, the feeding and draining vessels enlarge and undergo anatomical changes in their walls. The mechanisms responsible for these changes are not comprehensively understood, but the initiating event is clearly related to increased arterial flow, which is defined by the general principles of fluid dynamics: F = P/R A shunt exists between the high-pressure arterial system and the low-pressure venous system. This shunt is an anatomical pathological entity with low cerebrovascular resistance. A steal exists or, in the past did exist, as a consequence of the shunt and its low resistance. Arterial blood, destined for surrounding "normal" brain, is diverted from higherresistant vessels perfusing surrounding normal brain tissue into the low-resistant shunt. Venous hypertension occurs because of the increased blood flow through the shunt; the "afterload" or blood volume of the venous system is increased and, depending on the capacitance of the venous system. The Comprehensive Management of Arteriovenous Malformations of the Brain and Spine, ed. Average intraluminal pressure at various locations within the circulation under physiological conditions. Note the greatest drop in blood pressure occurs between the arteries and the arterioles. Consequently, small increases in the diameter of the arterioles result in significant decreases in resistance and, assuming that there is sufficient perfusion pressure, flow will increase dramatically. The ability of arteries to sense alteration of flow is an inherent property of the arterial wall [5]. This can be demonstrated in the laboratory with isolated perfused and pressurized brain arterioles, where acute increase in flow results in vasodilatation even in the absence of any parenchyma [6]. The above observations illustrate the arterial response to acute change in flow and may or may not be applicable to the chronic state. Most models are in rodents and are created by anastomosing a component of the carotid artery to the venous system and then studying the distant responses in brain and vascular tissue. Unfortunately, these surgically created fistulae, while ingenious, are not intracranial and may, therefore, not mimic the human condition. In addition, as has been recently recognized, rodent models have distinct limitations for simulating human diseases [12]. Moreover, there are recognized systemic abnormalities associated with kidney failure that make comparisons problematic [13]. With these caveats in mind, enlargement of the feeding arteries appears to be related to increase in flow and the ability of the vascular endothelium to sense change in flow and wall stress [14,15]. Shear stress (tau) is defined as a measure of the force of friction from a fluid acting on a body in the path of that fluid [7]. Like the similar cellular mechanisms in the inner ear, transformation of mechanical energy to a biological signal occurs in the endothelium. The biological signaling results in vascular smooth muscle growth and enlargement of the vessel diameter [14]. With prolonged time and stress, arteries undergo hypertrophy and changes that are characteristic of aging vessels: wall thickening, vascular smooth muscle hypertrophy, and, eventually, atherosclerosis [7,16]. These changes, either individually or in combination, alter the hemodynamic characteristics of the feeding arteries by varying wall stiffness, pulsatility, and shear stress. Comparable changes have been well documented in patients after traumatically or surgically induced arteriovenous fistulae [13]. Two different mechanisms can account for the recruitment of collateral blood flow: the low resistance of the shunt and brain tissue hypoperfusion. Depending on the degree of the shunt, increased flow may extend even to the cervical arteries. As noted above, the ability of arteries and arterioles to sense alteration of flow is an inherent property of the arterial wall. At the macro level of the cerebral circulation, flow is diverted toward the low resistance shunt and feeding arteries enlarge. A different mechanism appears to be responsible for the recruitment of flow from the external carotid. As a result of the diversion of arterial flow, the surrounding tissue is marginally perfused, simulating ischemic and/or hypoxic conditions. As in other ischemic or hypoxic conditions, the resultant chronic metabolic stress would be expected to elaborate substances such as adenosine, endothelial growth factor, and hypoxia-inducible factor 1, which induce blood vessel formation, growth, and eventually collateral flow from the external carotid circulation into the brain [20,21]. Venous hypertension, in the absence of ischemia, has also been shown experimentally to cause the elaboration of these factors [22]. Veins of the macrocirculation the venous system is characterized by low resistance, low intraluminal pressure, and a syncytial-like interconnection, which allows for large capacitance and redistribution of draining blood. In humans and other animals, two different types of venous system exist and have been characterized by their degree of compliance: large and small. The large compliant venous beds, such as the splanchnic and cutaneous circulations, have significant ability for storage of venous blood.