Anesthetic considertions for the PA Atient with systemic


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Anesthetic Considerations for the Patient with Systemic Lupus Erythematosus
Sharon T. , Carrillo* Emily , Gantz** Amir R. Baluch*** Rachel J. , Kaye**** and Alan D. Kaye*****
Systemic lupus erythematosus (SLE) is a complex disorder characterized by dysregulation of pathogenic autoantibodies and immune complexes that leads to multisystem chronic inflammatory processes1. SLE is not a rare condition; the estimated prevalence is 100 physician-diagnosed patients per 100,000 people. The disease may present at any age, although it primarily affects women of reproductive ages. The ratio of female to male patients is 9:1.
The prevalence of SLE is described as having an ethnic component, with black women affected 3 times more than whites2; in addition, blacks and Hispanics are reported to have higher rates of morbidity3. Although a classical presentation of SLE has been described, clinically there are many variations of the disease. For example, elderly patients tend to have a less-severe form involving fewer organ systems overall; men usually experience less photosensitivity but have a higher rate of mortality4,5.
SLE was first documented in the Middle Ages when it was termed lupus (“wolf” in Latin) to describe the appearance of the classical facial (malar) rash. It was suggested that the rash resembled the fur on the forehead and muzzle of the wolf. Others have suggested that the disease may have been named after a veil (loup) used by women in France to cover facial blemishes. It was not until 1872 that Móric Kaposi, a Hungarian dermatologist, began to recognize and describe the systemic manifestations of the disease6.
A groundbreaking advance in the study of lupus was made when Malcolm Hargraves, a hematologist at Mayo Clinic in 1948, described the lupus erythematosus or LE cell found in the bone marrow of patients. Ten years later, George Friou, MD, developed a test using fluorescent antihuman globulin demonstrating the antigen–antibody reaction, thus advancing the immunologic study of the disease7. Although SLE is largely attributed to autoimmune processes, its pathogenesis can be induced by drugs. This feature of SLE was discovered at the Cleveland Clinic in 1954, when a patient who was treated with hydralazine for hypertension subsequently developed SLE8.
Clinical Manifestations
Considerable variation exists in the clinical presentation of SLE, ranging from acute features with the classical malar, erythematous “butterfly rash” to a progressive fatal illness most commonly caused by complications of renal, cardiovascular, pulmonary, and central nervous

* Resident, Ochsner Clinic Foundation, in New Orleans, Louisiana. ** Medical Student, Texas College of Osteopathic Medical School, Fort Worth, Texas. *** Attending, Anesthesiologist, Metropolitan Anesthesia Consultants, Dallas, Texas. ***** Research Associate, Department of Anesthesiology, Louisiana State University School of Medicine,
Louisiana. ***** Professor and chairman, Department of Anesthesiology, Louisiana State University School of Medicine,
Louisiana. Corresponding author: Alan David Kaye, Email: [email protected]

New New

Orleans, Orleans,

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system (CNS) pathologies9. Across all age groups, SLE is characterized by chronic, inflammatory, multiorgan symptoms caused by immune complexes and antibodies against cell surface molecules or serum constituents10. The level of involvement of each organ system varies (Figure).
Mucocutaneous involvement is the most commonly reported clinical feature. It can appear as a rash (acute to chronic), alopecia, photosensitivity, and pathology of mucous membranes4. SLE patients commonly have manifestations found in other autoimmune diseases, such as Raynaud’s phenomenon, sclerodactyly, rheumatoid nodules, and erythema multiforme11. These manifestations are secondary to activation of the membrane attack complex and immune complex deposition12.
Musculoskeletal symptoms play a major role in the pathogenesis of SLE, affecting 53% to 95% of cases4. These include arthritic, arthropathic, myositic, and necrotic processes. Some complications arise from immunoglobulin deposition; others may be a result of corticosteroid treatment or hematologic pathogenesis.
Hematologic involvement is a common characteristic of SLE. It is defined variously as anemia, leukopenia, thrombocytopenia, and antiphospholipid syndrome. Most patients with SLE have anemia secondary to many causes, including immune-mediated hemolysis, chronic disease, renal insufficiency, aplastic anemia, hypersplenism, blood loss, myelodysplasia, myelofibrosis, and medication use. Thrombocytopenia in these patients can result from platelet destruction, microangiopathic hemolytic anemia, hypersplenism, bone marrow suppression, and thrombopoietin antibodies. SLE is commonly complicated by leukopenia-either neutropenia or lymphocytopenia. Antiphospholipid syndrome may coexist with SLE, causing thrombosis and vascular disease4.
Renal symptoms affect 40% to 70% of patients4. Mild, asymptomatic disorders of the urinary system affect many patients. A small percentage of cases progress to chronic renal insufficiency, a renal vasculitis syndrome, or severe lupus glomerulonephritis13.
Perhaps the most debilitating complications seen in SLE are those affecting the peripheral nervous system and CNS. The American College of

S. T. Carrillo et al.
Rheumatology (ACR) classifies these manifestations as neuropsychiatric systemic lupus erythematosus syndromes (NPSLE)14. The ACR has designated 19 syndromes within the NPSLE group. CNS syndromes include cerebrovascular disease, demyelinating syndrome, myelopathy, seizure disorder, psychosis, and aseptic meningitis. Peripheral nervous system syndromes include Guillain-Barré syndrome, mononeuropathy, myasthenia gravis, and cranial neuropathy4.
Cardiovascular involvement is variable. Chronic inflammation and autoantibodies accelerate atherosclerosis by injuring endothelial cells and altering lipoproteins15. The correlation between early, severe atherosclerosis and SLE, leads to an increased prevalence of coronary artery disease, myocardial infarction, and stroke in these patients16. Approximately 25% of patients with SLE develop pericarditis, whereas myocardial pathology is reported in less than 5% of patients4. Additionally, SLE increases the risk for valvular heart disease defined as aortic and mitral valve thickening, vegetations, regurgitation, and stenosis17.
Pulmonary involvement includes pleural, parenchymal, vascular, and muscular manifestations. The most common respiratory finding is pleuritic pain. Pleuritis is reported in more than 50% of patients with SLE. Clinically insignificant pleural effusions often are diagnosed. A more debilitating complication, although rare, is interstitial lung disease; its severity ranges from mild inflammation to extensive fibrosis18. Reports of other types of parenchymal involvement include acute pneumonitis secondary to alveolar wall necrosis, bronchiolitis obliterans, pulmonary hypertension, and infection due to immunosuppression19. Perhaps most worrisome is pulmonary hemorrhage secondary to inflamed capillaries, a relatively rare complication that has a mortality rate as high as 90%20. A late pulmonary consequence of SLE is diaphragmatic pathology. This complication, known as “shrinking lung syndrome”, causes decreased total lung capacity and volume21.
Infections play an important role in the morbidity and mortality in SLE. Disruption of normal immunity, chronic inflammation, and immunosuppressive therapy make these patients particularly susceptible. Complement deficiencies occur in SLE due to immune

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complexes activating the classical pathway. These deficiencies increase vulnerability to encapsulated bacteria and disseminated Neisseria infections22. Tuberculosis and Herpes Simplex Virus infections are also more prevalent among SLE patients. However, most often the respiratory and urinary tracts are involved by gram-negative and gram-positive bacteria23,24.
As supported by recent evidence, patients with SLE have an increased risk for cancer, including nonHodgkin’s lymphoma and lung, breast, and cervical malignancies. Although there is an association between malignancy and SLE, the pathogenic mechanisms are unknown. It has been suggested that genetic and environmental factors play a role25.
Pathogenesis
The pathogenesis of SLE is complex. Main factors include genetic patterns, gender, and environmental risks. Despite the different presentations of SLE, each patient shares a common dysregulation of autoantibody activity and an increased amount of immune complexes. Functionality at every level of the immune system is affected. Abnormalities in B cells, T cells, and immunoregulatory pathways have been described. [The unchecked production of these self-destructing molecules causes widespread inflammatory processes leading to a common theme of damaged organ systems]. The unchecked activation of inflammatory processes and resultant production of cytokines, most notably INF-α, are responsible for the systemic damage of organs26,27.
In SLE, many autoantibodies have a pathogenic role, targeting DNA, RNA, cell membrane structures, the cellular surface, and intracellular molecules1. The most prevalent self-destructing molecules are within the antinuclear antibody (ANA) group. The hypothesis supported by increasing evidence is that these antibodies originate from antinucleosomal antibodies28. A main concern is the effect of the antiDNA antibodies on renal parenchyma. The antibodies directly bind to or form complexes with various renal components, such as heparin sulfate proteoglycan, laminin, α-actinin, histone proteins, and glomerular basement membrane collagen29,30. In SLE, anti-DNA molecules also attack the CNS. These antibodies target

neurons and cause apoptosis, leading to cognitive impairment, altered mental status, and deterioration in mood31. Anti-phospholipid antibodies also contribute to neurologic dysfunction and are associated with an increased risk of strokes, seizures, and migraines32.
Other autoantibodies specific to cellular types cause complications in patients. A common selfdestructing molecule with up to 25% prevalence is the anti-Smith autoantibody, another ANA subtype. Highly specific for SLE, this autoantibody acts as an accelerator of disease1. Similarly, anti-Ro autoantibody has a particularly important part in the pathogenesis of SLE and is associated with nephritis, dermatitis, vasculitis, neonatal lupus, and Sjögren’s syndrome1.
With a variable severity of disease, some autoantibodies cause hematologic pathology; antibodies against platelets cause thrombocytopenia. More specifically, these antibodies are targeted against platelet cytoplasmic and surface components, including phospholipids and glycoproteins II and III33. The immunoglobulin G non-Rhesus antibody against an erythrocyte surface molecule contributes to SLE by causing hemolysis and anemia34. Additionally,
Table 1 Environmental Factors Associated With Pathogenesis of SLE
Ultraviolet B light Epstein-Barr virus Estrogen and prolactin:
Predilection for females (9:1 ratio, female: male) Lupus-inducing medications
Hydralazine Procainamide Isoniazid Hydantoins Chlorpromazine Methyldopa Penicillamine Minocycline Tumor necrosis factor-α inhibitors Interferon-α Dietary factors: Alfalfa sprouts and related sprouted foods containing canavanine, pristane Infectious agents other than Epstein-Barr virus Bacterial DNA Human retroviruses Endotoxins, bacterial lipopolysaccharides
SLE, systemic lupus erythematosus Adapted from reference 1.
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S. T. Carrillo et al.

Table 2 ACR Classification Criteria for SLE

Criteria

Description

ANA

Abnormal titer of ANA by immunofluorescence or equivalent assay at any time and in the absence of drugs known to be associated with drug-induced lupus syndrome

Arthritis

Non-erosive arthritis involving 2 or more peripheral joints and characterized by tenderness, swelling, or effusion

Discoid rash

Erythematous, raised patches with adherent keratotic scaling and follicular plugging; atrophic scarring occurs in older lesions

Hematologic disorder

Hemolytic anemia with reticulocytosis, or Leukopenia: <4,000/mm3, or Lymphopenia: <1,500/mm3, or Thrombocytopenia: <100,000/mm3 in the absence of contributing medications

Immunologic disorder

Anti-DNA: antibody to native DNA in abnormal titer, or Anti-Smith: presence of antibody to Smith nuclear antigen, or Positive finding of antiphospholipid antibodies based on: 1) abnormal serum concentration of IgG or IgM anticardiolipin antibodies; 2) positive test result for lupus anticoagulant using a standard method; or 3) false-positive serologic test for syphilis known to be positive for at least 6 months and confirmed by Treponema pallidum immobilization or fluorescent treponemal antibody absorption test

Malar rash

Fixed erythema, flat or raised, over the malar eminences, tending to spare the nasolabial folds

Neurologic disorder

Seizures in the absence of contributing medication or known metabolic derangements (eg, uremia, acidosis, or electrolyte imbalance) Psychosis in the absence of contributing medication or known metabolic derangements (eg, uremia, acidosis, or electrolyte imbalance)

Oral ulcers

Oral or nasopharyngeal ulceration, usually painless, observed by a physician

Photosensitivity

Skin rash as a result of unusual reaction to sunlight, by patient history or physician observation

Renal disorder

Persistent proteinuria, >0.5 g per day, >3+ if quantitation is not performed, or Cellular casts: may be red blood cell, hemoglobin, granular tubular, or mixed

Serositis

Pleuritis: convincing history of pleuritic pain or rub heard by physician or evidence of pleural effusion, or Pericarditis documented by ECG or rub or evidence of pericardial effusion

ACR, American College of Rheumatology; ANA, antinuclear antibody; ECG, electrocardiography; Ig, Immunoglobulin; SLE, systemic lupus erythematosus. Adapted from reference 29.

anticardiolipin antibody and lupus anticoagulant target phospholipids, inducing vascular thrombosis1.
Numerous genetic factors affect pathogenesis of SLE. Monozygotic twins appear to have an increased prevalence of SLE35. First-degree relatives have a reported 29-fold relative risk36. A predisposition to develop SLE is thought to involve expression of multiple genes and gene regions, including autoantibody production, several human leukocyte antigens, and non-leukocyte antigens1.
The clinical picture of each patient differs according to unique and multiple stimuli, and the pathogenesis of the disease may be influenced by a number of environmental factors1. These include exposure to viruses (most notably Epstein-Barr),

ultraviolet light, certain medications (including procainamide, hydralazine, isoniazid, hydantoins, chlorpromazine, methyldopa, penicillamine, minocycline, tumor necrosis factor blockers, and interferon-α), and certain dietary components (Table 1).
Diagnosis
The ACR has established clinical criteria for the diagnosis of SLE (Table 2). A patient must exhibit at least 4 of the following 11 features: serositis, manifested as pleuritis or pericarditis; oral ulcers, including nasopharyngeal lesions; arthritis; photosensitivity; hematologic abnormalities, including hemolytic anemia or any blood component deficiency; renal pathology, such as proteinuria or cellular casts;

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presence of immunologic disorders such as anti-Smith, anti-double-stranded DNA (anti-dsDNA), anti-histone, anti-U1RNP, anti-Ro/SSA, or anti-La/SSB; positive antinuclear antibodies; neurologic disorders; malar rash; and discoid rash. These standard criteria confer 95% specificity and 85% sensitivity for SLE diagnosis37. Positive ANA is the most sensitive and optimal test for SLE screening. However, ANA is commonly seen in other autoimmune disorders, while anti-dsDNA and anti-Smith antibodies are more specific to SLE38.
Diagnosing SLE may be a tedious process; however, many laboratory studies, imaging studies, and histologic tests are available. A Coombs’ test measures erythrocyte-specific antibodies in patients with anemia. Anti-histone screening may confirm druginduced lupus in a patient whose prescription history is pertinent1. Other tests are used to determine levels of certain biological markers to support the diagnosis. For example, an increased level of creatine kinase supports myositis; an elevated C-reactive protein level or erythrocyte sedimentation rate indicates an inflammatory state; and depressed levels of the complement proteins C3 and C4 suggest immune complex activity.
Lupus band test (LBT) is a useful diagnostic test that detects the deposition of immunoglobulins and complement in the dermal-epidermal junction by direct immunofluorescence. Specificity of LBT is very high, making it useful in the differentiation of SLE from other skin lesions, as well as, from other ANA positive diseases. A positive LBT in a patient without dermal involvement can aid in making the early diagnosis of SLE and can predict a decreased prognosis if involvement is seen in areas not exposed to UV-light39.
The use of various molecular biology techniques to test for antibodies coupled with the clinical picture may distinguish SLE from other connective tissue disorders or determine coexisting disease. For example, the presence of anti-Ro/SSA or anti-La/ SSB indicates Sjögren’s syndrome and is associated with neonatal lupus. Anti-RNP antibodies suggest scleroderma, whereas anti-cardiolipin antibodies have been described in the pathogenesis of antiphospholipid antibody syndrome1 (Table 3).

Table 3 Clinical Manifestations and Associated Autoantibodies in SLE

Manifestation

Autoantibody

Nephritis

Anti-dsDNA Anti-Ro Anti-C1q

Dermatitis

Anti-Ro Anti-dsDNA

Vasculitis

Anti-Ro

CNS

Anti-ribosomal P

Antineuronal

Anti-NR2

Hematologic Lymphopenia Hemolysis Thrombocytopenia Clotting

Antilymphocyte Antierythrocyte Antiplatelet Antiphospholipid

Fetal loss

Antiphospholipid

Sjögren’s syndrome

Anti-Ro

Neonatal lupus

Anti-Ro

CNS, central nervous system; dsDNA, double-stranded DNA; SLE, systemic lupus erythematosus Adapted from reference 1.

Prognosis and Treatment
Prior to advancements in screening tests, diagnostic laboratory studies, and treatment options, the prognosis was dismal for patients with SLE. Currently, the survival rate exceeds 90% in patients diagnosed 10 years previously40. Although the pathogenesis of SLE is different for each patient, there is an established correlation of increased mortality with infection, accelerated atherosclerosis, CNS involvement, and renal disease. For the younger patient, infection seems to be a main cause of death, whereas complications related to atherosclerosis decrease survival in older patients4. Etiologic factors that increase mortality include age greater than 50 years, male gender, and low socioeconomic status41.
Current therapeutic options for SLE are treatments directed at systemic inflammation, immunecell targets, signaling pathways, and cytokines. Antimalarial drugs, corticosteroids, cyclophosphamide, MMF, Methotrexate, and Aziothioprine are effective in suppressing inflammation. Agents that target B lymphocytes to prevent production of autoantibodies include rituximab (anti-CD20), epratuzumab (antiCD22), belimumab (anti–B-cell lymphocyte-activating factor [BAFF]), and atacicept (anti-BAFF and a
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proliferation-inducing ligand [APRIL]). Anti-cytokines, such as anti-TNF, anti-interleukins, and anti-INFα, interfere with immune cell signaling and activity42.
The treatment and management of patients with SLE varies. Disease severity and organ involvement determine a suitable treatment regimen. Treatment is induced during relapses in an effort to prevent exacerbations. Patients with mild SLE, defined by musculoskeletal and cutaneous involvement, generally are treated with antimalarials, glucocorticoids, and nonsteroidal anti-inflammatory agents. Patients in whom there is major organ involvement, including renal, hematologic, pulmonary, cardiac, and nervous systems, are considered to have moderate to severe SLE. These patients benefit from more intense treatment with immunosuppressive, cytotoxic, and biologic agents.4 Clinical guidelines set forth by the ACR recommend drug therapy with azathioprine, mycophenolate mofetil, cyclophosphamide, methotrexate, and cyclosporine, with appropriate monitoring for toxicity4. In addition, a new drug belimumab, a monoclonal antibody that inhibits B lymphocyte differentiation and autoreactivity, shows promising results in patients with active disease43.
Anesthetic Considerations Preoperative Assessment
Because of extensive, multiple organ dysfunction that can develop in SLE, the preoperative assessment of a patient with this disease may be extensive. Patient history, thorough physical examination, laboratory testing, and imaging are indicated. Cardiovascular function should be assessed with chest radiography, echocardiography, and electrocardiography to determine the presence of pericarditis, endocarditis, myocarditis, congestive heart failure, and conduction blocks.
In addition to cardiovascular evaluation, pulmonary function and arterial blood gas tests should be conducted if respiratory symptoms are present. Other complications such as lupoid hepatitis can be uncovered by liver function tests, a gastrointestinal series, and determination of albumin/globulin ratios and bilirubin levels. Anemia, thrombocytopenia, and leukopenia can be assessed by hematologic studies, including complete blood count, platelet count, prothrombin time, and partial thromboplastin time.

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For CNS involvement, electroencephalography and a computed tomography scan may be necessary. Renal involvement can be evaluated by urinalysis, renal ultrasound and scan, blood urea nitrogen level, and creatinine, albumin, and total serum protein levels44. Identifying specific organ dysfunctions and the clinical picture will determine the appropriate anesthetic plan (Table 4).
Intraoperative Assessment
There are many perioperative issues to consider in the patient with SLE-from organ pathology to anatomic change. As mentioned, multiple manifestations of the disease may alter anesthetic management of the patient. Renal or hepatic involvement may affect the metabolism and efficacy of common drugs, including IV and inhaled anesthetics, analgesics, neuromuscular inhibitors, cholinesterase inhibitors, and muscarinic antagonists. Patients treated with cyclophosphamide may require a longer period of anesthesia induction because of an inhibitory effect on cholinesterase that may lengthen the response to succinylcholine45. Intubation, extubation, and maintaining an airway may be difficult in some patients because of SLE-induced upper airway obstruction and laryngeal involvement10.
Airway Maintenance
Airway protection is a major concern in all patients undergoing anesthesia. Patients with SLE may have mucosal ulceration, cricoarytenoid arthritis, laryngeal pathology including recurrent laryngeal nerve palsy, or temporomandibular joint dysfunction that results in a difficult intubation10. Avoiding intubation when possible or using fiber-optic techniques are alternative approaches44.
Pulmonary
In patients with SLE, respiratory involvement may include acute pneumonitis, chronic alveolar infiltrates, and recurrent infectious pneumonia4. Perioperatively, pulmonary function and oxygenation should be carefully assessed. Avoidance of hypoxia, hypercapnia, and catecholamine release maintains pulmonary blood flow and reduces pulmonary vascular resistance. Arterial cannulation for blood gas analyses, and placement of a pulmonary artery catheter to assess

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Table 4 Preoperative Assessment of the Patient With SLE

System

Effects

Assessment by History

Physical Examination

Tests

Cardiovascular

Pericarditis Endocarditis Myocarditis CHF Conduction blocks

Chest pain Palpitations

Murmur Effusion Diastolic noncompliance Pericardial friction rub

ECG CXR Echocardiography

Respiratory

Infiltrates Restrictive PFTs h a-a gradient Atelectasis

Pleuritic pain Dyspnea Cough Hemoptysis

Friction rub Effusion Cyanosis Normal peak flow

CXR PFTs ABGs

Gastrointestinal

Perforated viscus Pseudo-obstruction Liver congestion Lupoid hepatitis

Nausea/vomiting Peritonitis Pancreatitis Abdominal pain Ileus

Dilated loops of bowel Peritoneal free air Hepatomegaly Jaundice

Gastrointestinal series LFTs Bilirubin level A/G ratio

Hematologic

Hemorrhage Thromboembolism Anemia

Bruising Thrombosis

Lymphadenopathy Splenomegaly Anemia

CBC Platelet count PT, PTT

Renal

Glomerulitis Nephrotic syndrome Renal insufficiency Renal failure

Polyuria Oliguria Hematuria Fever

Costophrenic tenderness Edema

Urinalysis Renal US Renal scan BUN, Cr, TP, albumin

CNS

Confusion

Paranoid states

Psychosis

EEG

Hallucinations

Hyperirritability

Nystagmus, ptosis, diplopia CT scan

Psychoses

Numbness

Aphasia

Neurologic, psychiatric

Seizures

Hemiparesis

Peripheral neuropathy

evaluations

Musculoskeletal and dermatologic

Vasculitis Symmetric arthritis Joint immobility Aseptic necrosis

Photosensitivity Atrophic/scarred lesions Ecchymosis Purpura Joint pain Immobility

Malar or butterfly rash Perioral ulcerations Reduced range of motion Hip pain

Hip x-rays Antinuclear antibody

a-a, alveolar-arterial; ABG, arterial blood gas; A/G, albumin/globulin; BUN, blood urea nitrogen; CBC, complete blood count; CHF, congestive heart failure; CNS, central nervous system; Cr, creatinine; CT, computed tomography; CXR, chest x-ray; ECG, electrocardiography; EEG, electroencephalography; LFT, liver function test; PFT, pulmonary function test; PT, prothrombin time; PTT, partial thromboplastin time; SLE, systemic lupus erythematosus; TP, total protein; US, ultrasound Adapted from Robinson DM. Systemic lupus erythematosus. In: Roizen MF, Fleisher LA, eds. Essence of Anesthesia Practice. 2nd ed. Philadelphia, PA: WB Saunders; 2002.

pulmonary hypertension, may be indicated44. A rare complication in these patients is alveolar hemorrhage, in which case pulmonary capillary exchange, oxygenation, and airway pressure must be monitored; suction should be readily available.
Renal
Glomerulitis, nephrotic syndrome, renal

insufficiency, and renal failure may develop. Renal involvement poses a significant challenge in patients with SLE and may alter standard administration of anesthetics44. Drugs requiring renal excretion, including some opioids, benzodiazepines, and neuromuscular blocking agents, may accumulate. The lingering, toxic metabolites lead to prolonged sedation, paralysis, and an increased recovery period. Additionally, the kidneys
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or other organ systems may be further damaged. In cases of extreme end-organ damage, the use of remifentanil and cisatracurium-both metabolized via processes that are end organ-independent-is indicated.
Cardiovascular
Premature and accelerated atherosclerosis increases the risk for cardiovascular disease46. Patients are predisposed to potentially catastrophic events such as intraoperative myocardial infarction. Every effort should be made to maintain hemodynamic stability.
Management of the Case Presented
A detailed medical history of the patient was obtained, and a physical examination completed. Her airway was characterized as Mallampati class II with good cervical range of motion. Her lungs were clear to auscultation; heart sounds were regular without murmurs. Other findings of the physical examination were within normal limits, except for alopecia, which was moderate.
After a discussion with the patient about the risks

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and benefits of general anesthesia, regional anesthesia, and supplemented local anesthesia, the latter was chosen. After IV administration of 2 mg of midazolam and 50 mcg of fentanyl, the surgeon locally injected a mixture of bupivacaine and lidocaine. A propofol infusion of 40 mcg/kg per minute was started. The patient also received 4 mg of ondansetron. The procedure lasted 45 minutes. The patient was discharged to undergo dialysis, and later to home.
Conclusion
SLE is a complicated autoimmune disease with variable systemic manifestations. Because of the complexity and potentially wide-ranging clinical presentations of SLE, anesthetic management of patients is challenging. The inherent heterogeneity of SLE necessitates extensive preoperative assessments of patients, in addition to obtaining detailed histories and physical examinations. Careful anesthetic planning and intraoperative monitoring of all affected organ systems-particularly renal, pulmonary, and cardiovascular function-are required.

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Anesthetic considertions for the PA Atient with systemic