Harvey Jay Cohen, MD

• Professor of Medicine
• Walter Kempner Distinguished Professor of Medicine, in the School of Medicine
• Emeritus Director, Center for the Study of Aging & Human Development
• Faculty Research Scholar of DuPRI's Center for Population Health & Aging
• Member of the Duke Cancer Institute

https://medicine.duke.edu/faculty/harvey-jay-cohen-md

An obstruction of tomless in most cases because of the rich orbital collaterals treatment myasthenia gravis buy coversyl 4 mg lowest price, the posterior inferior cerebellar artery or an obstruction but its transient embolic obstruction can lead to amaurosis of the vertebral artery just before it branches to this vessel fgax-sudden and briefloss of vision in one eye medications knee buy coversyl 8mg free shipping. There may be a contralateral grasp refex treatment modalities purchase 8 mg coversyl free shipping, paratonic artery leads to coma with pinpoint pupils symptoms narcolepsy cheap coversyl 8 mg free shipping, faccid quadri? rigidity medicine 6 year course order cheap coversyl line, and abulia (lack of initiative) or frank confusion treatment ketoacidosis purchase coversyl 4mg. With partial basilar artery occlusion, there may be behavioral disturbances are conspicuous. Bilateral anterior diplopia, visual loss, vertigo, dysarthria, ataxia, weakness cerebral infarction is especially likely to cause marked or sensory disturbances in some or all of the limbs, and behavioral changes and memory disturbances. In patients with hemiplegia anterior cerebral artery occlusion proximal to the junction of pontine origin, the eyes are often deviated to the para? with the anterior communicating artery is generally well lyzed side, whereas in patients with a hemispheric lesion, tolerated because of the collateral supply from the other side. Middle cerebral artery occlusion leads to contralateral When the small paramedian arteries arising from the basi? hemiplegia, hemisensory loss, and homonymous hemiano? lar artery are occluded, contralateral hemiplegia and sen? pia (ie, bilaterally symmetric loss of vision in half of the sory defcit occur in association with an ipsilateral cranial visual felds), with the eyes deviated to the side of the nerve palsy at the level of the lesion. If the dominant hemisphere is involved, global Occlusion of any of the major cerebellar arteries pro? aphasia is also present. It may be impossible to distinguish duces vertigo, nausea, vomiting, nystagmus, ipsilateral limb this clinically from occlusion of the internal carotid artery. If the superior cerebellar artery is involved, the con? be considerable swelling of the hemisphere during the first tralateral spinothalamic loss also involves the face; with 72 hours. For example, an infarct involving one cerebral occlusion of the anterior inferior cerebellar artery, there is hemisphere may lead to such swelling that the function of ipsilateral spinothalamic sensory loss involving the face, the other hemisphere or the rostral brainstem is disturbed usually in conjunction with ipsilateral facial weakness and and coma results. Imaging sia and to contralateral paralysis and loss of sensations in the arm, the face and, to a lesser extent, the leg. Screening for antiphospholipid antibod? hemorrhage, (3) recent arterial puncture at a noncompress? ies (lupus anticoagulants and anticardiolipin antibodies); the ible site, (4) previous intracranial hemorrhage, (5) intracra? factor V Leiden mutation; abnormalities of protein C, pro? nial neoplasm or arteriovenous malformation, (6) recent tein S, or antithrombin; or a prothrombin gene mutation is intracranial or intraspinal surgery, (7) active internal bleed? indicated only if a hypercoagulable disorder is suspected (eg, ing or bleeding diathesis (eg, platelets less than 100,000/ a young patient without apparent risk factors for stroke). While atrial fbrillation include minor stroke, seizure at stroke onset, pregnancy, will be discovered in approximately 10% of patients with major surgery within previous 14 days, gastrointestinal or ischemic stroke during their hospitalization, it is estimated urinary tract hemorrhage within previous 21 days, and that an arrhythmia will be found in an additional 10% with myocardial infarction within previous 3 months. Echocardiography patients with large vessel occlusion (about 20% of patients (with agitated saline contrast) should be performed in cases with acute ischemic stroke) are eligible for embolectomy, of nonlacunar stroke to exclude valvular disease, lef-to-right which must be performed within 6 hours of stroke onset. Blood cultures should be Early management of a completed stroke otherwise performed if endocarditis is suspected but are not required requires general supportive measures. Examination of the cerebrospinal fuid is not stroke care unit has been shown to improve outcomes, always necessary but may be helpful if cerebral vasculitis or likely due to early rehabilitation and prevention of medical another infammatory or infectious cause of stroke is sus? complications. Maintenance of an adequate cere? Management is divided into acute and chronic phases, the bral perfusion pressure helps prevent further ischemia. The most important initial stroke onset) for malignant middle cerebral artery infarc? determination is the time at which the patient was last nor? tions reduces mortality and improves functional outcome. However, if the systolic pressure exceeds 220 mm Hg, it can be lowered All patients should be hospitalized, preferably in a stroke using intravenous labetalol or nicardipine with continuous care unit. Guidelines for the early management of patients pressure augmentation is usually not necessary in patients with acute ischemic stroke: a guideline for healthcare profes? sionals from the American Heart Association/American with relative hypotension but maintenance of intravenous Stroke Association. There is generally Stroke Association focused update ofthe 2013 guidelines for no advantage in delay, and the common fear of causing the early management of patients with acute ischemic stroke hemorrhage into a previously infarcted area is misplaced, regarding endovascular treatment: a guideline for healthcare since there is a far greater risk of frther embolism to the professionals from the American Heart Association/American Stroke Association. In all cases, early mobilization and active rehabilitation are Spontaneous, nontraumatic intracerebral hemorrhage in important. Occupational therapy may improve morale and patients with no angiographic evidence of an associated motor skills, while speech therapy may help expressive vascular anomaly (eg, aneurysm or angioma) is usually due dysphasia or dysarthria. The pathologic basis for hemorrhage is following stroke, access to food and drink is typically probably the presence of microaneurysms that develop on restricted until an appropriate swallowing evaluation; the perforating vessels in hypertensive patients. Hypertensive head of the bed should be kept elevated to prevent aspira? intracerebral hemorrhage occurs most frequently in the tion. Urinary catheters should not be placed and, if placed, basal ganglia, pons, thalamus, cerebellum and less com? removed within 24-48 hours. Hemor? rhages usually occur suddenly and without warning, often the prognosis for survival after cerebral infarction is better during activity. In the elderly, cerebral amyloid angiopathy than after cerebral or subarachnoid hemorrhage. Arteriovenous malformations are an impor? embolectomy are also at least 30% more likely to achieve tant cause of intracerebral hemorrhage in younger patients. Loss of consciousness after a Other causes of nontraumatic intracerebral hemorrhage cerebral infarct implies a poorer prognosis than otherwise. Patients who have had a cerebral infarct are at risk for cular coagulation), anticoagulant therapy, liver disease, high additional strokes and for myocardial infarcts. Bleeding is primarily into the subarachnoid space when the recurrence rate by 30% among patients without a car? it occurs from an intracranial aneurysm, but it may be diac cause for the stroke who are not candidates for carotid partly intraparenchymal as well. Nevertheless, the cumulative risk of recur? cause for cerebral hemorrhage can be identifed. Clinical Findings recovery is unlikely should receive palliative care (see Chapter 5). When to Refer ness is initially lost or impaired in about one-half of All patients should be referred. Intracranial pressure may require toms and signs then develop, depending on the site of the monitoring and osmotic therapy. With hypertensive hemorrhage, there is gen? be required in patients with intraventricular hemorrhage erally a rapidly evolving neurologic defcit with hemiplegia and acute hydrocephalus. A hemisensory disturbance is also present when a superfcial hematoma in cerebral white matter is with more deeply placed lesions. With lesions of the puta? exerting a mass effect and causing incipient herniation. The treatment of of nausea and vomiting, dysequilibrium, headache, and underlying structural lesions or bleeding disorders depends loss of consciousness that may terminate fatally within on their nature. When to Refer cases, however, the onset and course are intermediate, and All patients should be referred. When to Admit hemiplegia; peripheral facial weakness; ataxia of gait, limbs, or trunk; periodic respiration; or some combination All patients should be hospitalized. Laboratory and Other Studies A complete blood count, platelet count, prothrombin and partial thromboplastin times, and liver and kidney func. General Considerations tion tests may reveal a predisposing cause for the hemor? Between 5% and 10% of strokes are due to subarachnoid rhage. Occasional patients with Patients should be admitted to an intensive care unit for aneurysms have headaches, sometimes accompanied by observation and supportive care. The systolic blood pres? nausea and neck stiffness, a few hours or days before mas? sure should be lowered to 140 mm Hg. This has been attrib? should be treated with platelet transfusion; the specific uted to "warning leaks" of a small amount of blood from the threshold for treatment and the goal platelet count after aneurysm. Symptoms and Signs min K, or specific reversal agents (eg, protamine for hepa? rin, idarucizumab for dabigatran). Its onset is with sudden headache of a severity underlying coagulopathy has not improved survival or never experienced previously by the patient. The systolic sciousness is regained, the patient is often confused and blood pressure should be lowered to 140 mm Hg until the irritable and may show other symptoms of an altered aneurysm is secured. Neurologic examination generally reveals to prevent seizures, but the evidence of benefit is con? nuchal rigidity and other signs of meningeal irritation, ficting (see Table 24-3). However, most are the major aim of treatment is to prevent further hem? asymptomatic or produce only nonspecific symptoms until orrhage. The risk of further hemorrhage from a ruptured they rupture, at which time subarachnoid hemorrhage aneurysm is greatest within a few days of the first hemor? results. A higher risk of subarachnoid hemorrhage is asso? rhage; approximately 20% of patients will have further ciated with older age, female sex, "nonwhite" ethnicity, bleeding within 2 weeks and 40% within 6 months. Defini? hypertension, tobacco smoking, high alcohol consumption tive treatment, ideally within 2 days of the hemorrhage, (exceeding 150 g per week), previous symptoms, posterior requires surgical clipping of the aneurysm or endovascular circulation aneurysms, and larger aneurysms. Focal neuro? treatment by interventional radiologists; the latter is some? logic signs are usually absent but, when present, may relate times feasible even for inoperable aneurysms and has a either to a focal intracerebral hematoma (from arteriove? lower morbidity than surgery. Imaging severe complications, so monitoring is necessary, usually in an intensive care unit. Transcranial Doppler ultrasound examined for the presence of blood or xanthochromia may be used to screen noninvasively for vasospasm, but before the possibility of subarachnoid hemorrhage is conventional arteriography is required to document and treat vasospasm when the clinical suspicion is high. Cerebral arteriography is undertaken to determine the Nimodipine has been shown to reduce the incidence of source of bleeding. After bral arteriography are necessary because aneurysms are often multiple, while arteriovenous malformations may be surgical obliteration of all aneurysms, symptomatic vaso? spasm may also be treated byintravascular volume expan? supplied from several sources. The procedure allows an interventional radiologist to treat an underlying aneurysm sion and induced hypertension; transluminal balloon angioplasty of involved intracranial vessels is also helpful. If arteriograms show no abnormality, the examination should Aspirin provides no benefit. Prophylactic administration be repeated after 2 weeks because vasospasm or thrombus ofintravenous magnesium sulfate does not change overall may have prevented detection of an aneurysm or other clinical outcomes. Laboratory and Other Studies enough to require temporary, and less commonly pro? the cerebrospinal fuid is bloodstained. Electro-cardio? longed or permanent, intraventricular cerebrospinal fuid graphic evidence of arrhythmias or myocardial ischemia shunting. Renal salt-wasting is another complication of has been well described and probably relates to excessive subarachnoid hemorrhage that may develop abruptly dur? sympathetic activity. Peripheral leukocytosis and transient ing the first several days of hospitalization. Daily measurement of the serum All patients should be hospitalized andseenbya neurolo? sodium level allows for the early detection ofthis complica? gist. Hypopituitarism may occur as a late complication of por and coma are applied to comatose patients. Differentiation between traumatic tap and aneu? rysmal subarachnoid hemorrhage: prospective cohort study. They may be associated ology, natural history, management options, and familial with polycystic kidney disease and coarctation of the aorta. Arteriovenous Malformations in more distal vessels and ofen at the cortical surface. The most significant complication of intracranial aneurysms is a subarachnoid hemorrhage, which is discussed in the pre? ceding section. A higher risk of subarachnoid hemorrhage is associated with older age, female sex, "non-white" eth? Sudden onset of subarachnoid and intracerebral nicity, hypertension, tobacco smoking, high alcohol con? hemorrhage. Aneurysms may cause a focal neurologic deficit by com? pressing adjacent structures. General Considerations tomatic or produce only nonspecific symptoms until they rupture, at which time subarachnoid hemorrhage results. Arteriovenous malformations are congenital vascular mal? Its manifestations, complications, and management were formations that result from a localized maldevelopment of outlined in the preceding section. Imaging that are fed by multiple vessels and involve a large part of Definitive evaluation is by angiography (bilateral carotid the brain to lesions so small that they are hard to identif and vertebral studies), which generally indicates the size at arteriography, surgery, or autopsy. In approximately 10% and site of the lesion, sometimes reveals multiple aneu? of cases, there is an associated arterial aneurysm, while rysms, and may show arterial spasm if rupture has 1-2% of patients presenting with aneurysms have associ? occurred. Clinical presentation usually adequate if operative treatment is under consider? may relate to hemorrhage from the malformation or an ation because lesions may be multiple and small lesions are associated aneurysm or may relate to cerebral ischemia due sometimes missed. Regional maldevelop? scan shows no evidence of bleeding but subarachnoid ment of the brain, compression or distortion of adjacent hemorrhage is diagnosed clinically, a lumbar puncture cerebral tissue by enlarged anomalous vessels, and progres? should be performed to examine the cerebrospinal fuid sive gliosis due to mechanical and ischemic factors may for blood. Supratentorial lesions-Most cerebral arteriovenous certainty and to determine its anatomic features so that malformations are supratentorial, usually lying in the terri? treatment can be planned. Initial symptoms consist include bilateral opacification of the internal and external of hemorrhage in 30-60% of cases, recurrent seizures in carotid arteries and the vertebral arteries. Arteriovenous 20-40%, headache in 5-25%, and miscellaneous com? malformations tyically appear as a tangled vascular mass plaints (including fo cal deficits) in 10-15%. Up to 70% of with distended tortuous afferent and efferent vessels, a arteriovenous malformations bleed at some point in their rapid circulation time, and arteriovenous shunting. Arteriovenous malformations that have bled once are detailed anatomy of any focal lesion identified by these more likely to bleed again. Hemorrhage is commonly intra? means are delineated by angiography, especially if opera? cerebral as well as into the subarachnoid space, and it has a tive treatment is under consideration. Laboratory and Other Studies seizures may accompany or follow hemorrhage, or they may be the initial presentation, especially with frontal or Electroencephalography is usually indicated in patients parietal arteriovenous malformations. Headaches are espe? presenting with seizures and may show consistently focal cially likely when the external carotid arteries are involved or lateralized abnormalities resulting from the underlying in the malformation. Treatment In patients presenting with subarachnoid hemorrhage, examination may reveal an abnormal mental status and Surgical treatment to prevent further hemorrhage is justi? signs of meningeal irritation. Additional findings may help fed in patients with arteriovenous malformations that localize the lesion and sometimes indicate that intracranial have bled, provided that the lesion is accessible and the pressure is increased. Surgical treatment possibility of a cerebral arteriovenous malformation, but is also appropriate if intracranial pressure is increased and bruits may also be found with aneurysms, meningiomas, to prevent further progression of a focal neurologic defcit. Bruits are drug treatment is usually sufficient, and operative treat? best heard over the ipsilateral eye or mastoid region and are ment is unnecessary unless seizures cannot be controlled of some help in lateralization but of no help in localization. Absence of a bruit does not exclude the possibility of arte? Defnitive operative treatment consists of excision ofthe riovenous malformation. Two other techniques for the treatment of arteriovenous malformations may also be clinically incon? intracerebral arteriovenous malformations are injection of spicuous but sometimes lead to cerebellar hemorrhage. Stereotactic radiosurgery is also useful in bleeding has recently occurred, helps localize its source, the management of inoperable cerebral arteriovenous and may reveal the arteriovenous malformation. The paired posterior spinal arteries, Intracranial venous thrombosis mayoccur in association by contrast, are supplied by numerous arteries at different with intracranial or maxillofacial infections, hypercoag? levels of the cord. Spinal cord hypoperfusion may lead to a ulable states, polycythemia, sickle cell disease, and cya? central cord syndrome with distal weakness of lower notic congenital heart disease and in pregnancy or motor neuron type and loss of pain and temperature during the puerperium.

Acute adrenal crisis is more commonly seen in primary adrenal insufficiency than in secondary adrenal Shah M et al medications depression buy coversyl paypal. It pressed the other adrenal gland; (4) following sudden may present at any age and accounts for one-third of cases destruction of the pituitary gland (pituitary necrosis) keratin treatment buy coversyl 8 mg otc, or of Addison disease in boys symptoms 9 days after iui cheap coversyl online american express. Aldosterone deficiency occurs when thyroid hormone is given to a patient with adrenal in 9% symptoms of ebola best order coversyl. Psychiatric symptoms insufficiency; (5) following injury to both adrenals (by often include mania medicine numbers generic 8 mg coversyl fast delivery, psychosis treatment head lice coversyl 4mg free shipping, or cognitive impairment. Rare causes of adrenal insufciency include lymphoma, metastatic carcinoma, coccidioidomycosis, histoplasmosis. With such autoimmunity, adrenal Congenital adrenal insuffciency occurs in several function decreases over several years as it progresses to conditions. A varied spectrum of associated diseases may be ciency, achalasia, alacrima, nasal voice, autonomic dys? seen in adulthood, including hypogonadism, hypothyroid? fnction, and neuromuscular disease of varying severity ism, pernicious anemia, alopecia, vitiligo, hepatitis, malab? (hyperrefexia to spastic paraplegia). Congenital adrenal hypoplasia causes 20-40 years, usually women (female: male ratio is 3: 1). The combination of Addison disease and genetic defects in the enzymes responsible for steroid syn? hypothyroidism is known as Schmidt syndrome. Due to defective cortisol synthesis, patients have may also have vitiligo, alopecia areata, Sjogren syndrome, or variable degrees of adrenal insufciency and increased celiac disease. The most common enzyme defect is P450c21 cious anemia (4%); and, rarely, autoimmune hypophysitis, (21-hydroxylase deficiency). P450c21 (classic congenital adrenal hyperplasia) manifest a Infection is a relatively rare cause of Addison disease in deficiency of mineralocorticoids (salt wasting) in addition the United States but is common in much of the world. Hyperten? Tuberculosis is the most common infection of the adrenals, sion commonly develops in older adult patients with clas? and parallels its prevalence worldwide. Testicular adrenal rests sis and other infections are rare causes, particularly in can be found in 44% of men with the condition. It may occur in Patients with defcient P450c17 (17-hydroxylase defi association with major surgery or trauma, presenting about ciency) have varying degrees of cortisol deficiency with 1 week later with pain, fever, and shock. The absence of adrenal insufficiency may be mistaken for chloasma sex hormones results in primary amenorrhea. Undiagnosed adrenal insufficiency can cause Patients with deficient P450cll (1 1-hydroxylase defi? intrauterine growth retardation and fetal loss. Pregnant ciency) present at birth with partial virilization and ambig? women with undiagnosed adrenal insufficiency can expe? uous genitalia in genetically female infants, childhood rience shock from adrenal crisis, particularly during the virilization in both sexes, and virilization and reduced fer? first trimester, concurrent illness, labor, or postpartum. Most patients have hypertension and Patients with preexistent type 1 diabetes experience variable degrees of cortisol deficiency. The diagnosis is more frequent hyoglycemia with the onset of adrenal established with elevated serum levels of 11-deoxycortico? insufficiency, such that their insulin dosage must be sterone and 11-deoxycortisol. Drugs that cause primary adrenal insufficiency include Acute adrenal crisisis an immediate threat to life. Nau? mitotane (for adrenocortical carcinoma) and abiraterone sea, vomiting, fever, dehydration, and profound hypoten? acetate (a P450cl7inhibitor used for prostate cancer). Among patients with chronic adrenal often delayed, since many early symptoms are nonspecifc. Fevers and lymphoid tissue hyperplasia A plasma cortisol less than 3 mcg/dL (83 nmoi! Blood pressure is usually have stimulated serum cortisol levels less than 20 meg low and orthostatic; about 90% have systolic blood pres? (550 pmol/L). For patients receiving corticosteroid treat? sures under 110 mm Hg; blood pressure over 130 mm Hg ment, hydrocortisone must not be given for at least 8 hours is rare. L) in 100% of patients with adrenal insuffciency but the most, but nonexposed areas darken as well. Hyperpig? also in about 15% of the population, so the test is very mentation is often especially prominent over the knuckles, sensitive but not specifc. Nipples and areolas of serum antibodies to 21-hydroxylase helps secure the tend to darken. The skin also darkens in pressure areas, diagnosis of autoimmune adrenal insufficiency. Con? Salt-wasting congenital adrenal hyperplasia due to versely, patches of autoimmune vitiligo can be found in 21-hydroxylase deficiency is usually diagnosed at birth in about 10% of patients. The diagno? In pregnancy, undiagnosed adrenal insufficiency is sis of adrenal insufficiency is made as above. Young men with idiopathic Addison disease are screened for X-linked adrenoleukodystrophy by determin. Complications ing plasma very long-chain fatty acid levels; affected Any of the complications of the underlying disease (eg, patients have high levels. General Measures noncalcified adrenals are seen in autoimmune Addison Patients with Addison disease mustbethoroughly informed disease. Patients are advised to wear a medi? related to metastatic or granulomatous disease. The hyperpigmentation therapy for most patients with Addison disease involves may be confused with that due to ethnic or racial factors. Some patients respond better son disease should be considered in any patient with to prednisone (available in 1 mg tablets) or methylpred? unexplained hyotension, but acute adrenal insufficiency nisolone (4 mg tablets) in doses of about 2-4 mg orally in must be distinguished from other causes of shock (eg, sep? the morning and 1-2 mg in the evening. Plenad? Unexplained weight loss, weakness, and anorexia may ren (5 or 20 mg modified-release tablets) is a once-daily be mistaken for occult cancer. Nausea, vomiting, diarrhea, dual-release preparation of hydrocortisone that may be and abdominal pain may be misdiagnosed as intrinsic gas? administered once daily in the morning (usual dose range trointestinal disease. Acute adrenal insuffciency must be is 20-30 mg); it is not available in the United States. The neurologic vary substantially and should not be used to determine manifestations of Allgrove syndrome and adrenoleukodys? dosing. The dose of glucocorticoid should be raised in case trophy (especially in women) may mimic multiple sclero? of infection, trauma, surgery, stressful diagnostic proce? sis. With infection, note that hyperpigmentation, but hemochromatosis may in fact be rifampin increases the clearance of hydrocortisone and the cause of Addison disease. During the third trimester of pregnancy, glucocorti? cause frank adrenal insufficiency. Hyponatremia is seen in many other conditions (eg, hypothyroidism, diuretic use, heart failure, cirrhosis, vom? 2. Mineralocorticoid replacement therapy-Fludrocorti? iting, diarrhea, severe illness, or major surgery). In the However, one retrospective Swedish study of 1675 patients presence of postural hypotension, hyonatremia, or hyper? with Addison disease found an unexpected increase in all? kalemia, the dosage is increased. For example, patients with adreno? mia, or hypertension ensues, the dose is decreased. Patients with adrenal tuberculosis have doses appropriate for stress, fudrocortisone replacement is a serious systemic infection that requires treatment. Some patients cannot tolerate fudrocorti? nal crisis can occur in patients who stop their medication sone and must substitute NaCl tablets to replace renal or who experience stress such as infection, trauma, or sur? sodium loss. However, some patients feel residual fatigue, ment did not improve fatigue, cognitive problems, or sex? despite glucocorticoid and mineralocorticoid replacement. Acute adrenal crisis therapy-If acute adrenal crisis is For patients with acute adrenal crisis, rapid treatment is suspected but the diagnosis of adrenal insufficiency is not usually lifesaving. However, if adrenal crisis is unrecog? yet established, blood is drawn for routine emergencylabo? nized and untreated, shock that is unresponsive to fuid ratory tests and blood cultures, as well as serum cortisol replacement and vasopressors can result in death. Without waiting for the results, treat? ment is initiated immediately with hydrocortisone phos? phate or hydrocortisone sodium succinate 100-300 mg Allolio B. Thereafter, 25288693] hydrocortisone is continued as intravenous infusions of Charmandari E et a!. Psychological morbidity and impaired quality administered empirically while waiting for the results of of life in patients with stable treatment for primary adrenal initial cultures. The patient must also betreated for electro? insufciency: cross-sectional study and review of the litera? lyte abnormalities, hypoglycemia, and dehydration, as ture. Most patients ultimately require hydrocortisone twice daily (10-20 mg in am; 5-10mg in pm). Somepatients never require fudrocortisone or become edematous at doses of more than 0. General Considerations extremities eventually develop in most patients with Cush? ing syndrome. Muscle atrophy causes weakness, with dif? the term Cushing "syndrome" refers to the manifestations ficulty standing up from a seated position or climbing of excessive corticosteroids, commonly due to supraphysi? stairs. Patients may also experience backache, headache, ologic doses of corticosteroid drugs and rarely due to hypertension, osteoporosis, avascular necrosis of bone, spontaneous production of excessive corticosteroids by the acne, superficial skin infections, and oligomenorrhea or adrenal cortex. Cases of spontaneous Cushing syndrome amenorrhea in women or erectile dysfunction in men. Mental symptoms is caused by a benign pituitary adenoma that is tyically may range from diminished ability to concentrate to smaller than 5 mm and usually located in the anterior pitu? increased lability of mood to frank psychosis. Hypokalemia and have microscopic metastases that can only beinferred from hyperpigmentation are commonly found in this group. Most such Glucose tolerance is impaired as a result of insulin resis? cases are due to a unilateral adrenal tumor. Polyuria is present as a result of increased free water adenomas are generally small and produce mostly cortisol; clearance; diabetes mellitus with glycosuria may worsen it. The dexamethasone suppression test is the easiest adrenal macronodular adrenocortical disease is a rare screening test for Cushing syndrome. L, fuorometric the Carney complex, an autosomal dominant condition assay) or less than 1. However, 8% of established patients with pituitary Cushing disease have dexameth? asone-suppressed cortisol levels less than 2 mcgldL (55. Therefore, when other clinical criteria suggest hypercortisolism, further evaluation is warranted even in A. Symptoms and Signs the face of normal dexamethasone-suppressed serum the manifestations of Cushing syndrome vary consider? cortisol. Early in the course of the disease, patients frequently primidone) and rifampin accelerate the metabolism of complain of fatigue or reduced endurance but may have dexamethasone, causing a lack of cortisol suppression by few, if any, of the physical stigmata described below. Differential Diagnosis an indwelling intravenous line established in advance for the blood draw. Alcoholic patients can have hypercortisolism and many clinical manifestations of Cushing syndrome. Most such lesions are wasting and extraordinarily high urine free cortisol levels benign adrenal adenomas, but an adrenal carcinoma is found in anorexia. Although the overwhelming major? empiric replacement-dose hydrocortisone postoperatively. The cosyntropin test becomes than 4 em in diameter is detected in a patient without a abnormal by 2 weeks following successful pituitary surgery. Masses 3-4 em in diameter may be resected ifthey glucocorticoid replacement until a cosyntropin stimulation have suspicious features (heterogeneity or irregularity). Patients 15 minutes after contrast; a reduction (washout) of40% or must have repeated evaluations for recurrent Cushing dis? more is consistent with a benign adrenal adenoma. In particular, patients with hypertension or any pos? nificant morbidity and mortality. All (even normoten? stereotactic radiosurgery, which normalizes urine free cor? sive) patientswith an adrenal incidentaloma require testing tisol in 70% ofpatients within a mean of 17 months, com? for pheochromocytoma with plasma fractionated free pared with a 23% remission rate with conventional metanephrines. Pituitary radiosurgery can also be used to treat Nelson syndrome, the progressive enlargement of. Patients with Cushing syndrome of any etiology face a high Benign adrenal adenomas may be resected laparo? complication rate after treatment and all patients require scopically if they are smaller than 6 em in diameter; cure is intensive clinical care and close follow-up. However, most patients experi? their families must receive thorough education about the ence prolonged secondary adrenal insufciency. Affected patients should also receive vacci? or genetic changes at chromosome 2p16. Such patients nations against influenza, pneumococcus, and herpes zos? require regular screening for testicular and thyroid tumors ter. All patients undergoing surgery should have prophylaxis and frequent echocardiogram screening for atrial against venous thromboembolism. Surgical Therapy tive secondary adrenal insufficiency is a good prognostic Pituitary Cushing disease is best treated with transsphe? sign, with an increased chance that the tumor was com? noidal selective resection of the pituitary adenoma. However, the postop? an experienced pituitary neurosurgeon, reported remission erative presence of detectable cortisol indicates metastases rates range from 65% to 90%. Most patients are treated postoperatively occurs frequently, so serum sodium should be monitored with mitotane for 2-5 years, since it improves survival. Unfortunately, only half with secretory adrenalcortical carcinoma whose hyercor? the patients are able to reach these levels due to side effects. Replacement hydrocortisone or Themanifestations ofCushing syndrome regress with time, prednisone should be started when mitotane doses reach but patients are ofen left with residual cognitive or psychi? 2 g daily. The replacement dose of hydrocortisone starts at atric impairment, muscle weakness, osteoporosis, and 15 mg in the morning and 10 mg in the afternoon, but sequelae from vertebral fractures. Continued impaired must often be doubled or tripled because mitotane quality oflife is more common in women compared to men. Other chemotherapy regimens have been used, usu? adenoma experience a 5-year survival of95% and a 10-year ally adding etoposide to mitotane. If that cannot be nonsuppressed serum cortisol is less than 2 mcg/dL done, laparoscopic bilateral adrenalectomy is usually rec? (55 nmol! Medical treatment with a combination of mortality remains particularly higher for patients with mitotane (3-5 g/24 h), ketoconazole (0. Recur? tension, nausea, fatigue, arthralgias, myalgias, pruritus, rence of hypercortisolism may occur as a result of growth and faking skin.

First medicine 20 generic coversyl 8 mg mastercard, recall that diabetc anterior segment neo does tend to be a bit more indolent relatve to neo from other causes symptoms of appendicitis purchase generic coversyl line. Plus if you have injected bevacizumab medicine venlafaxine coversyl 8 mg lowest price, you have some real fexibility as far as how you treat the patent symptoms ear infection safe coversyl 4 mg. Rather than fring in 2 administering medications 8th edition purchase coversyl once a day,000 fast spots treatment diverticulitis discount coversyl 8 mg otc, as you might do for progressive angle neovascularizaton from a central retnal vein occlusion, you can ofen do the laser in a divided dose. This can be important because these can be frail eyes?you can run into complicatons more easily than in a typical diabetc eye. More aggressive disease calls for more aggressive treatment with even higher numbers, especially if the pressure is elevated. It is important to get good control of the vessels, especially if the patent may need glaucoma surgery; you don?t want a lot of bleeding or neovascular invasion of your favorite seton. As a result, anterior segment neovascularizaton becomes less aggressive for some patents once a seton is placed. Things get tricky if you identfy the neovascularizaton, but the patent does not have any symptoms. This almost always involves fancier techniques, such as indirect laser or even cryotherapy, especially if the view is poor. If a cataract is obscuring the view, avoid just popping it out and waitng for the eye heal before moving on to the laser. If there is extensive proliferatve disease back there, your injectons may stop the anterior segment neovascularizaton but you may also be pulling the retna of as the posterior vessels contract. Patents like that should be referred so everything can be cleaned out with a vitrectomy. If patents have a lot of aggressive anterior neo, though, you really don?t have much choice; this is just another thing to be aware of if you are trying to tackle such sick eyes. They need to know that you are dealing with an eye that in the old days would ofen end up blind and painful and in a jar. Your treatments will likely prevent that, but they cannot expect to have a fun tme or a great visual outcome. They may need multple injectons with no obvious visual beneft, and the heavy laser and possible glaucoma surgery will take a toll on their vision. Patents also need to understand that although there are potental complicatons, the biggest danger is that the treatments may not work. And if that happens, they will get worse as they are being treated, and if things really go south they may even end up enucleated. And, to repeat for the second tme in one paragraph, if they don?t have a lot of symptoms, they are going to really be unhappy with you and your crazy treatments because they were just fne before you started in on them. Patents can really misinterpret what you are saying when you talk about enucleatons. In other words, say The eye can become so painful that you will beg us to take it out of your head. Risk of missing angle neovascularizaton by omitng screening gonioscopy in patents with diabetes mellitus. Intracameral Avastn dramatcally resolves iris neovascularizaton and reverses neovascular glaucoma. Human Ciliary Epithelium as a Source of Synthesis and Secreton of Vascular Endothelial Growth Factor in Neovascular Glaucoma. Mark Twain Unless you are reading this as you lug your laser to the nearest free clinic, it is likely that you will be involved in some sort of economic transacton when you treat a patent. If you are in a developed country that has frst-dollar universal coverage, you can stop reading this right now because this secton does not apply to you. If you are in a developing country, then you do need to worry about this stuf because there are insufcient healthcare resources available to cover the populaton. There are some suggestons about what to do at the end of this chapter (and at the end of Chapter 5). If you are living in America, reportedly the richest country on earth, you really need to read this because you will inevitably have patents with no way to aford the care they need. There is an inclinaton to surrender your control in this area to whatever large bureaucratc structure you happen to be a part of?this way some other functonary has to fuss with droll maters like billing and collectons while you concentrate on the noble task of being a physician. Try not to think like this?it can result in your patents making extremely bad decisions. Being diabetc, it is hard to get a job with good insurance, and individual insurance can be very expensive. Many diabetcs learn to survive without insurance by paying for their medical care on an intermitent basis and/or with the help of charity clinics. This is not ideal, and this approach usually breaks down when they start to develop complicatons and need more expensive care (which is where you come in). But even if they do have insurance, recent developments in the marketplace have made many types of insurance? almost useless. The classic example is a high-deductble plan, where the patent may be responsible for the frst several thousand dollars of their care. If one is healthy and well of, these plans are no big deal, but if you have a chronic disease then it is almost the same as being uninsured as people struggle to pay of huge accumulated debt. So imagine you are an otherwise healthy diabetc, but now you are getng proliferatve disease. Some doctor is telling you that even though you don?t have any symptoms, you need to sit down and get pounded with a laser that will hurt, maybe blur your vision, and certainly won?t help you see any beter. Then you go talk to the billing person, and they tell you that all of this bliss is going to cost thousands of dollars that you don?t have. You may be totally caring and empathetc, but a relatvely disinterested bean counter can completely undo things by making patents visualize eatng cat food in order to pay for something that they don?t want to do anyway. They will then return in one to two years with severe proliferatve disease and tractonal detachments that may not be fxable. It turns out that this works out well for the accounts receivable department, because now the patent is blind and they are at least eligible for Medicaid?some blood can fnally be squeezed out of their partcular turnip. You?and the Great Ophthalmologic Court in the Sky judging our actons?should be somewhat less than sanguine about how the system allows this to happen. This scenario simply should not occur, but it does, due to the nature of human beings and the nature of the healthcare system. You are in a positon to stop this from happening, given that only you know how desperately such a patent needs treatment. Most patents, especially patents in this situaton, will immediately assume that any tme a doctor talks about money, it means that the doctor is simply performing a wallet biopsy prior to putng on the big squeeze. Remind them that they need the treatment to avoid blindness, and you want to make sure that they get treated properly whether they can pay or not. The alternatves available to you depend on how much control you have over your billing. It is likely that if you are reading this book you are in training or just startng your career and you may not have much control over how patents are billed. If cost is an issue for the patent you should try to take a moment to explain to the billing person the severity of the situaton, making sure they know to go as easy as possible on the patent. This could be dangerous ground?for instance, Medicare considers doing a procedure without billing for it to be fraud, no mater how noble the cause. Hopefully someone somewhere will realize how uterly illogical all of this is and the system will be fxed. This eliminates any fnancial stress, and ofering to do something regardless of payment is a very powerful way to demonstrate to a patent the importance of the treatment. And if you need to do injectons, you may well be able to get free drugs from the makers of Lucents and Eylea. You may actually fnd that such a patent will remain quite devoted to you, and you may fnd that the whole process is rather rewarding on a number of warm and fuzzy levels that are beyond the scope of this book. If such an approach does not ft into your worldview, consider a more cynical argument for this policy: if you can keep them functoning in society, they will certainly think of you when they do eventually get insurance and may need electve procedures. They will also speak very highly of you to all of their friends, family, and other doctors and, yes, there may be a risk of inundatng your ofce with their equally uninsured acquaintances?but it is far more likely that the long-term goodwill you acquire in the community is going to transcend any short-term irregularites in your cash fow. The botom line on the botom line is that it is hard enough to convince diabetcs to show up for evaluaton and treatment without adding fnancial impediments. This chapter really applies only to doctors in situatons where patents may have a signifcant fnancial burden when undergoing treatment. As mentoned at the beginning of this secton, doctors in developing countries have a related problem, and it has to do with the fact that there are tons of patents in need of help, but there are no resources to help with paying for their care. If you are in this situaton, it turns out that there are a lot of organizatons out there that are interested in helping?you just have to start making the efort to contact them. It is very likely that someone, somewhere has already faced the problems you are having, and has fgured out a way to deal with it?and ofen quite successfully. The world is full of places that have skillfully combined capitalism and altruism to create very efectve, self-sustaining programs that reward both the populaton and the doctors who take the tme to go beyond their borders and ask for help. To get back my youth I would do anything in the world, except take exercise, get up early, or be respectable. You will be amazed at how you are largely wastng your tme if your patent is noncompliant. When you see how a set of eyes can improve when a patent gets religious about control, and how your treatments work way beter in such patents, you will realize that it is defnitely worth the tme to rag on your patents about their systemic status. You can give the sweetest intravitreal injectons and do the fnest lasers, but if you don?t emphasize systemic control with both patents and their physicians you are functoning at the Epsilon-Minus Semi-Moron level of doctorness. Figure 1: this patent had some mild grid laser to the center, but most importantly she really began to take care of herself once she realized that the writng was on the wall. Note the almost total resoluton of the multple hemorrhages and the overall healthier appearance of the fundus afer several years of beter systemic control. The most obvious one is glucose control, and the quickest way to assess this is to ask the patent what their hemoglobin A1c is. Almost all patents will check their sugars periodically, and they may even remember some of their results (especially the best ones), but a sporadic sampling of glucose levels does not convey the overall level of control. In developed countries there is no reason why a patent should not be aware of their hemoglobin A1c level, although sometmes it helps if you call it the three-month glucose test? if a patent does not recognize the test by name. Simply fnding out whether they have heard of the test is useful?if they do not know what you are talking about you know you have a really big problem. Such a patent needs to be educated about the test and you need to express your concerns to their primary care physician. You can even order the test yourself to be sure it is done and to motvate both the patent and their doctor. Most patents will know the about the test, and even if they do not know their actual number, they can tell you whether their doctor was happy with the results. Red blood cells last two to three months, and because they do not manufacture fresh hemoglobin, measuring the fracton of hemoglobin that has been glycosylated ofers an idea of the average glucose level over that tme period. The test is basically a variaton of the hemoglobin electrophoresis that one might do to evaluate for sickle cell disease, but one is looking for the hemoglobin fracton that has the glucose moiety, rather than hemoglobin S. The translaton of the A1c value into the corresponding glucose value varies with the testng method, and the actual result implies a range of values. Table 1 shows the average? glucose value that can be inferred from the hemoglobin A1c. A general rule of thumb is to shoot for a hemoglobin A1c as close to normal as possible without inducing excess hypoglycemia. Note that there is some controversy about how aggressive to be in patents with Type 2 diabetes. Recent studies suggest that intensive control can help slow down retnal and renal disease, but there was an overall increase risk of mortality in the intensive control group. The point is that you?as an ophthalmologist?should not dictate a specifc A1c level to the patent. A1c (%) Mean Blood Sugar (mg/dl) Table 1: Hemoglobin A1c Values and Corresponding Average 6 126 Glucose Level 7 154 Note that even the good? value of 7% 8 183 corresponds to a consistently elevated glucose. If you know a patent has bad systemic control, then your ophthalmic management may need to change. For instance, a patent with poor control should be checked more frequently because they are very likely to progress faster. You may also need to be more aggressive about treatment decisions when patents have borderline ophthalmic disease. Of greatest signifcance is the fact that a bad hemoglobin A1c means that you really have to make sure the patent has appropriate expectatons with any treatment that you do, whether it be laser, injectons or cataract surgery. Patents with poor control have a worse prognosis for everything, and they must understand that although your interventons will slow things down, the odds are they will tend to worsen, even with perfect treatment. If you have a lot of patents that do not know their A1c level, you can buy or lease your own machine to get immediate results. The test only requires a fnger stck, and the machine does not require sophistcated training. Be careful how you harangue the patent about improving Figure 2: Rate of retnopathy progression relatve to mean their control. There are other systemic factors that can play a role in progression of retnopathy. Four signifcant ones are hypertension, renal failure, lipid abnormalites and anemia. For instance, it is not unusual to see patents who present with progressive renal failure and macular edema, only to have the edema resolve without treatment as soon as the renal failure is treated. Hypertension is partcularly well studied?the sine qua non coming from the United Kingdom Prospectve Diabetes Study Group. It makes sense to5 routnely check the blood pressure on diabetc patents, especially if it is not clear how good the patent is with their medical follow up. Yes, you might end up writng more leters, and you might actually have to check some blood pressures yourself, and you may even need to do general medical things like putng the patent in a room to calm down and then rechecking their blood pressure. All this is worth it, though, because you will be surprised at the number of patents who are not as well controlled as they tell your technicians. It also helps to encourage patents to talk to their doctors about home blood pressure monitoring in the same way they monitor their glucose?automatc blood pressure cufs are efectve and cheap.

Determination of appropriate metabolic compensation After 6-12 hours treatment zit purchase coversyl on line amex, the primary increase in Pco2 evokes a may reveal an associated metabolic disorder (see Mixed renal compensation to excrete more acid and to generate Acid-Base Disorders) symptoms during pregnancy generic coversyl 4mg with visa. Treatment Hypotension Severe anemia Treatment is directed toward theunderlying cause medications depression coversyl 4mg on line. Infection Hyperventilation is usually self-limited since muscle weak? Trauma Tumor ness caused by the respiratory alkalemia will suppress Pharmacologic and hormonal stimulation ventilation medicine quotes purchase coversyl 4 mg with mastercard. The Xanthines severity of hypocapnia in critically ill patients has been Pregnancy (progesterone) associated with adverse outcomes treatment of scabies buy cheap coversyl 8 mg online. Patients with hypoglycemia symptoms bowel obstruction purchase line coversyl, starvation ketosis, or ketoacidosis being treated with insulin may require 5% dextrose-containing solutions. Insensible water loss should be considered in febrile In acute cases (hyperventilation), there is light-headedness, patients. Dir, M D Kidney disease can be discovered incidentally during a Various findings on the urinalysis are indicative of routine medical evaluation or with evidence of kidney dys? certain patterns of kidney disease. The initial approach in both situations should be to disorders that are not intrinsic to the kidney, such as lim? assess the cause and severity of renal abnormalities. In all ited effective blood fow to the kidney or obstruction ofthe cases, this evaluation includes (1) an estimation of disease urinary outfow tract. Heavy proteinuria and lipiduria physical examinations, though equally important, are vari? are consistent with the nephrotic syndrome. The presence able among renal syndromes-thus, specific symptoms and of hematuria with dysmorphic red blood cells, red blood signs are discussed under each disease entity. Disease Duration termed "muddy brown casts") and renal tubular epithelial Kidney disease may be acute or chronic. White injury is worsening of kidney function over hours to days, blood cells, including neutrophils and eosinophils, white resulting in the retention of nitrogenous wastes (such as blood cell casts (Table 22-1), red blood cells, and small urea nitrogen) and creatinine in the blood. Retention of amounts of protein can be found in interstitial nephritis these substances is called azotemia. Hematuria and proteinuria are discussed more important for diagnosis, treatment, and outcome. Anemia (from low kidney erythropoi? etin production) is rare in the initial period of acute kidney A. Significant proteinuria is a sign of an underlying kidney abnormality, usually glomerular in origin when more than. Less than 1 g/day can be due to multiple causes A urinalysis can provide information similar to a kidney along the nephron segment, as listed below. The urine should be examined levels, abnormal urinary sediment, or evidence of systemic within 1 hour afer collection to avoid destruction of illness (eg, fever, rash, vasculitis). Urinalysis includes a dipstick examina? There are several reasons for development ofprotein? tion followed by microscopic assessment if the dipstick has uria: (1) Functional proteinuria is a benign process stem? positive fndings. Urinary specific gravity is found in people under age 30 years, usually results in uri? often reported. Microscopy provides examination offormed nary protein excretion of less than 1 g/day. The clinical sequelae of proteinuria are discussed in the section Type Significance Nephrotic Spectrum Glomerular Diseases below. Hyaline casts Concentrated urine, febrile disease, after strenuous exercise, in the course of B. Hematuria diuretic therapy (not indicative of renal disease) Hematuria is signifcant if there are more than three red cells per high-power field on at least two occasions. It is Red cell casts Glomerulonephritis usually detected incidentally by the urine dipstick exami? White cell casts Pyelonephritis, interstitial nephritis nation or clinically following an episode of macroscopic (indicative of infection or inflammation) hematuria. The diagnosis must be confrmed via micro? Renal tubular cell Acute tubular necrosis, interstitial nephritis scopic examination, as false-positive dipstick tests can be casts caused by myoglobin, oxidizing agents, beets and rhubarb, Coarse, granular Nonspecific; can represent acute tubular hydrochloric acid, and bacteria. Transient hematuria is casts necrosis common, but in patients younger than 40 years, it is less Broad, waxy casts Chronic kidney disease (indicative of stasis often of clinical signifcance due to lower concern for in enlarged collecting tubules) malignancy. Extrarenal causes are addressed in Chapters 23 and 39; most worrisome are urologic malignancies. Renal causes 8-hour overnight supine urinary protein excretion, which account for approximately 10% of cases and are best con? should be less than 50 mg. Urinary pro? lar causes include immunoglobulin A (IgA) nephropathy, tein electrophoresis will exhibit a discrete protein peak. The simplest method is to collect a random plasma proteins, are freely flterable across the glomerulus, urine sample. The ratio of urinary protein concentration to and are neither secreted nor reabsorbed along the renal urinary creatinine concentration ([U r tcino ]/[Ucrc tininca ]) cor? p tubules. The formula used to determine the renal clearance relates with a 24-hour urine protein collection (less than of a substance is 0. The benefit of a urine protein-to-creatinine ratio UxV C = is the ease of collection and the lack of error from overcol? p lection or undercollection of urine. In a 24-hour urine col? lection, a fnding of greater than 150-160 mg is abnormal, where C is the clearance, U and P are the urine and plasma and greater than 3. With stable kidney function, creatinine pro? Catabolic states (gastrointestinal bleeding, corticosteroid use) duction and excretion are equal; thus, plasma creatinine High-protein diets concentrations remain constant. Of ues of creatinine clearance from the Cockcroft-Gault note, the creatinine clearance is the traditional estimation equation. It is synthesized mainly in the liver and is the end One way to measure creatinine clearance is to collect a product of protein catabolism. Urea is freely fltered by the timed urine sample and determine the plasma creatinine glomerulus, and about 30-70% is reabsorbed in the renal level midway through the collection. Unlike creatinine clearance, which overestimates prolonged urine collection is a common source of error. The creatinine clearance decreased renal perfusion (heart failure, renal artery declines by an average of 0. If a patient is unwilling to or decline in urinary output, which correlates with progno? accept therapy based on biopsy findings, the risk of biopsy sis. Absolute contraindications include an kg/h over 12 hours or longer; stage 3 as a 3-fold or greater uncorrected bleeding disorder, severe uncontrolled hyper? increase in serum creatinine or decline in urinary output to tension, renal infection, renal neoplasm, hydronephrosis, less than 0. In the absence offunctioning kidneys, Prior to biopsy, patients should not use medications that serum creatinine concentration will tpically increase by prolong clotting times and should have well-controlled 1-1. Blood work should include a hemoglobin, rhabdomyolysis, serum creatinine can increase more rapidly. Patients Patients with acute kidney injury of any type are at higher should be closely monitored when the hematocrit is lower risk for all-cause mortality according to prospective cohorts, than baseline by more than 3% at 6 hours postbiopsy. When a percutaneous needle the uremic milieu of acute kidney injury can cause non? biopsy is technically not feasible and kidney tissue is specific symptoms. When present, symptoms are often due deemed clinically essential, a closed biopsy via interven? to uremia or its underlying cause. Uremia can cause nau? tional radiologic techniques or open biopsy under general sea, vomiting, malaise, and altered sensorium. General Considerations decreased organic and nonorganic acid clearance) are often Acute kidney injury is defned as a rapid decrease in kidney noted. Hyperphosphatemia occurs when phosphorus can? function, resulting in an inability to maintain acid-base, not be secreted by damaged tubules either with or without fluid, and electrolyte balance and to excrete nitrogenous increased cell catabolism. The 2012 Kidney Disease Improving Global Out? decreased erythropoietin production overweeks, and asso? comes Clinical Practice Guidelines for Acute Kidney Injury ciated platelet dysfnction is typical. Prerenal causes are the most common etiology of acute Arrhythmias and valvular disorders can also reduce cardiac kidney insults and injury, accounting for 40-80% of cases, output. If reversed quickly with restoration of renal whether acute kidney injury is due to prerenal or intrinsic blood flow, renal parenchymal damage often does not renal causes. If hypoperfusion persists, ischemia can result, caus? important, and urinalysis can be helpful. Thus, patients with prerenal excessive diuresis, extravascular space sequestration, pan? causes should have a low fractional excretion percent of creatitis, burns, trauma, and peritonitis. Oliguric patients with intrinsic kid? Changes in vascular resistance can occur systemically ney dysfunction typically have a high fractional excretion of with sepsis, anaphylaxis, anesthesia, and afterload-reducing sodium (greater than 1-2%). After reversal of the underlying process, acute tubular necrosis if sodium intake and excretion are these patients often undergo a postobstructive diuresis, relatively low. For was created and validated to assess the difference between example, patients with retroperitoneal fbrosis from tumor oliguric acute tubular necrosis and prerenal states. Prompt treatment of obstruction within days by the cause of acute kidney injury may not be accurately catheters, stents, or other surgical procedures can result in predicted. Acute kidney injury due to glomerulonephritis partial or complete reversal of the acute process. Intrinsic Acute Kidney Injury Treatment of prerenal insults depends entirely on the Intrinsic renal disorders account for up to 50% of all cases causes, but maintenance of euvolemia, attention to serum of acute kidney injury referred to a nephrologist. Intrinsic electrolytes, and avoidance ofnephrotoxic drugs are bench? dysfunction is considered after prerenal and postrenal marks of therapy. When to Refer Postrenal causes are the least common reason for acute If a patient has signs of acute kidney injury that have kidney injury, accounting for approximately 5-10% of not reversed over 1-2 weeks, but no signs of acute ure? cases, but important to detect because of their reversibility. Occasionally, postrenal uropathies can occur when a single If a patient has signs ofpersistent urinary tract obstruc? kidney is obstructed if the contralateral kidney cannot tion, the patient should be referred to a urologist. In men, benign prostatic hyperplasia for acute intervention, such as emergent urologic interven? is the most common cause. Less common practice guideline on acute kidney injury in the individual causes are blood clots, bilateral ureteral stones, urethral patient. Summary of clinical practice guidelines for stones or strictures, and bilateral papillary necrosis. Polyuria can occur in the setting of partial obstruction with resultant tubular dysfunction and an inability to appropriately reabsorb salt and water loads. On examination, the patient may have an enlarged prostate, distended bladder, or mass detected on pelvic examination. Urine sediment with pigmented granular casts because extensive intrinsic renal damage has not occurred. Patients with acute kidney injury and suspected postre? Acute kidney injury due to tubular damage is termed nal insults should undergo bladder catheterization and "acute tubular necrosis" and accounts for approximately ultrasonography to assess for hydroureter and 85% of intrinsic acute kidney injury. Ischemic acute kidney injury is characterized not lead to increased rates of renal dysfunction in this setting. In some small studies, N-acetylcysteine given before tubular damage with low effective arterial blood flow to the and after contrast decreases the incidence of dye-induced kidney can result in tubular necrosis and apoptosis. However, a large prospective randomized occurs in the setting of prolonged hypotension or hypox? controlled trial showed no benefit of N-acetylcysteine in emia, such as volume depletion or shock. Acetylcysteine is a thiol? periods of hypoperfusion, which are exacerbated by vasa? containing antioxidant with little toxicity whose mecha? dilating anesthetic agents. With little harm and possible benefit, administering acetylcysteine 600 mg orally every A. Exogenous Nephrotoxins 12 hours twice, before and afer a dye load, for patients Aminoglycosides cause some degree of acute tubular with preexisting risk factors at risk for acute kidney injury, necrosis in up to 25% of hospitalized patients receiving is a reasonable strategy. Nonoliguric kidney injury 1200 mg prior to an emergent procedure, has shown typically starts to occur after 5-10days ofexposure. Predis? beneft compared with placebo and may be a good option posing factors include underlying kidney damage, volume if a patient needs contrast dye urgently. Aminoglycosides can remain have shown a beneft using sodium bicarbonate (154 mEq/L, in renal tissues for up to a month, so kidney function may intravenously at 3 mL! However, others have shown sodium Gentamicin and tobramycin are equally nephrotoxic; bicarbonate was not superior to sodium chloride when streptomycin is the least nephrotoxic of the aminoglyco? using similar administration regimens. Other nephrotoxic sides, likely due to the number of cationic amino side agents should be avoided during the day before and after chains present on each molecule. The largest ongoing randomized trial Amphotericin B is typically nephrotoxic after a dose of to date is investigating intravenous normal saline versus 2-3 g. This causes a type I renal tubular acidosis with bicarbonate and N-acetylcysteine versus placebo to prevent severe vasoconstriction and distal tubular damage, which contrast-induced nephropathy in a 2x2 design, with a can lead to hypokalemia and nephrogenic diabetes insipi? result expected for 2019. Vancomycin, intravenous acyclovir, and several Cyclosporine toxicity is usually dose dependent. It cephalosporins have been known to cause acute tubular causes distal tubular dysfunction (a type 4 renal tubular necrosis. Regular blood level Radiographic contrast media may be directly nephro? monitoring is important to prevent both acute and chronic toxic. With patients who are taking cyclosporine new-onset acute kidney injury in hospitalized patients. It to prevent kidney allograft rejection, kidney biopsy is often probably results from the synergistic combination of direct necessary to distinguish transplant rejection from cyclo? renal tubular epithelial cell toxicity and renal medullary sporine toxicity. Predisposing factors include advanced age, pre? reducing the dose or stopping the drug. Lower volumes of contrast with lower osmolality are recom? Endogenous nephrotoxins include heme-containing prod? mended in high-risk patients. Prevention should be the goal when using these which is freely fltered across the glomerulus. The mainstay of therapy is a liter of intravenous bin is reabsorbed by the renal tubules, and direct damage 0. Distal tubular obstruction from pigmented casts contrast administration-cautiously in patients with pre? and intrarenal vasoconstriction can also cause damage. Isotonic intravenous volume this type of kidney injury occurs in the setting of crush repletion is superior to hypotonic intravenous solutions injury, or muscle necrosis from prolonged unconscious? which are both superior to oral solutions in small studies. Patients may complain of muscular nonoliguric, with oliguria portending a worse prognosis. The globin moiety ofmyoglo? bin will cause the urine dipstick to read falsely positive for hemoglobin: the urine appears dark brown, but no red cells. With lysis ofmuscle cells, patients also become Treatment is aimed at hastening recovery and avoiding hyperkalemic, hyperphosphatemic, and hyperuricemic. Preventive measures should be taken to Hypocalcemia may ensue due to phosphorus and calcium avoid volume overload and hyperkalemia.

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