Rheumatologic Disease in the Intensive Care Unit

Published on 07/03/2015 by admin

Filed under Critical Care Medicine

Last modified 22/04/2025

Print this page

rate 1 star rate 2 star rate 3 star rate 4 star rate 5 star
Your rating: none, Average: 0 (0 votes)

This article have been viewed 1005 times

Chapter 58 Rheumatologic Disease in the Intensive Care Unit

Lynda S. Tilluckdharry, MB, BCh, BAO, LRCP&SI , Christine Haas Jones, MD

1 A critically ill patient is seen with an acute hot, swollen joint. What is the next step in management? What are the most common organisms found in a septic joint?

Aspiration of the joint should be performed immediately to rule out a septic joint, crystalline disease, or other inflammatory forms of arthritis. The synovial fluid should be sent for cell count and differential, Gram stain, culture, and crystalline analysis. High fevers and elevated inflammatory markers: erythrocyte sedimentation rate (ESR), C-reactive protein, and white cell counts, may be found in both infection and crystalline arthropathy. It is important to remember that septic arthritis and crystal-induced arthropathy can occur concurrently in a joint.

In all age and risk groups, the most common causative organisms of septic arthritis are Staphylococcus aureus and Streptococci strains. In nursing home patients, intravenous abusers, elderly people, and patients with recent orthopedic procedures, consider methicillin-resistant S. aureus. These populations are also susceptible to mixed bacterial infections, gram-negative organisms, fungal infections, and unusual organisms. In young adults, consider Neisseria gonorrhoeae as a cause of septic arthritis. Treatment includes prompt removal of purulent material from the joint space and initiation of appropriate intravenous antibiotics targeting suspected organisms. Serial arthrocentesis or open surgical drainage may be necessary.

2 List the risk factors for the development of septic arthritis

image Diabetes

image Alcoholism

image Joint prosthesis

image Intravenous drug abuse

image Skin infections or cutaneous ulcers

image Recent joint surgery or intraarticular corticosteroid injection

image Age: elderly or young

image Previous joint pathologic condition, for example, rheumatoid arthritis (RA), osteoarthritis, or crystal-induced arthropathy

3 Name the common risk factors for gout

image Surgery

image Dehydration

image Drugs such as diuretics

image High purine intake in diet

image Trauma

image Infections

image Renal insufficiency

image Excess alcohol intake

4 How do you interpret synovial fluid analysis?

See Table 58-1.

Table 58-1 Synovial fluid analysis

image

5 What specific precautions should be taken when performing intubation in a patient with RA?

Cervical spine disorders occur in 30% to 50% of patients with RA. The most common presentation of cervical spine arthritis is C1-C2 subluxation or atlantoaxial subluxation (AAS). Vertical and subaxial subluxation occurs less commonly. It is prudent for providers to use caution when performing any manipulations of the cervical spine, particularly endotracheal intubation in patients with RA. Spinal cord compression due to C1 and C2 instability may lead to neurologic deficits or death. Lateral and flexion cervical spine radiographs or magnetic resonance imaging should be obtained before intubation in the following situations:

image RA duration >3 years

image Long-term use of corticosteroid

image Severe peripheral joint deformities from RA

image Male sex

image Neck pain

image Risk factors for osteoporosis

image Prior cervical spine subluxation

image Clinical evidence of cervical myelopathy

If clinical or radiographic evidence of subluxation exists and intubation is required, an anesthesiologist should be present during the procedure. In patients with AAS, subluxation is worsened with cervical flexion and reduced by cervical extension. Cricoarytenoid arthritis may also complicate endotracheal intubation. These patients may present with symptoms of tracheal pain, stridor, dysphonia, and shortness of breath (see Fig. 58-1).

image

Figure 58-1 Rheumatoid arthritis of the cervical spine.

(From Firestein GS, Budd RC, Harris ED, et al: Kelley’s Textbook of Rheumatology, 8th ed, vol 1. Philadelphia, Saunders, 2008, p 810.)

6 What is scleroderma renal crisis (SRC)? When should this diagnosis be considered, and how is it confirmed?

SRC will occur in 15% of patients with systemic sclerosis (SSc). SRC is a medical emergency and presents with an abrupt onset of hypertension (>150/85 mm Hg) and acute renal failure (>30% reduction of glomerular filtration rate). SRC can precede the diagnosis of SSc, and patients can initially be seen with normal blood pressures.

image Clinical symptoms include headaches, visual disturbances from hypertensive retinopathy, seizures, encephalopathy, fever, general malaise, pulmonary edema. Less commonly, patients may have arrhythmias, myocarditis, and pericarditis.

image Laboratory tests typically show an elevated creatinine level, microangiopathic hemolytic anemia, and thrombocytopenia. Urinalysis may show mild proteinuria, hematuria, and granular casts.

7 Who is at risk for SRC, and what are risk factors indicating poor prognosis? What treatment should be initiated in SRC?

The major risk factors for the development of SRC are early diffuse cutaneous systemic sclerosis, positive antinuclear antibody (ANA) with a diffuse speckled pattern, rapidly progressive skin disease, and recent corticosteroid use. Patients with positive anti-fibrillarin, anti-U1RNP, and RNA polymerase I and II antibodies are at a higher risk for SRC.

Poor prognosis for recovery from SRC is associated with the following:

image Male sex

image Age > 50 years

image Persistent renal failure

image Initial presentation with normal blood pressure

Treatment should include early therapy with angiotensin-converting enzyme inhibitors (ACEi) such as captopril and lisinopril. To avoid hypoperfusion, ensure gradual decrease in blood pressure with other antihypertensives such as calcium channel blockers, nitrates, and β-blockers. Transient mild increases in creatinine level are common and are not an indication to stop the ACEi. Many patients will require supportive care with dialysis, and kidney function may take up to 3 years to improve. Plasma exchange can be considered in patients with microscopic angiopathy.

8 What conditions can be associated with a positive ANA test in a critical care patient?

image Systemic lupus erythematosus (SLE) or drug-induced lupus

image Mixed connective tissue disease

image Autoimmune liver disease

image Systemic sclerosis

image Sjögren syndrome

image RA

image Polymyositis (PM)

image Malignancy

image Thyroid disease

image Miscellaneous: normal population (5%-10%), elderly (20%), medications

9 How do you interpret a positive ANA test? What additional investigations should be ordered if there is a positive ANA test?

In isolation, a positive ANA test should not be used to make a specific diagnosis, and a negative ANA does not exclude an autoimmune condition. In most laboratories an ANA titer of >1:40 is considered positive, and clinically significant titers are usually >1:160.

Additional investigations that should be obtained include double-stranded DNA (dsDNA), SS-A (Ro) and SS-B (La) antibodies, Smith antigen (Sm), ribonuclear protein (RNP), centromere antibody, urinalysis, complement levels (C3 and C4), and a complete blood cell count with differential, which may show leucopenia and lymphopenia.

10 What clinical findings in a patient whose condition is deteriorating would prompt the consideration of SLE?

image Unexplained fevers

image Unexplained neurologic symptoms such as altered mental status, seizures, psychosis (lupus cerebritis)

image Renal abnormalities with proteinuria and cellular casts (lupus nephritis)

image Hematologic disorders such as hemolytic anemia

image Serositis such as pericardial effusion and pleural effusion

image Multiorgan failure

MD SOAP’N HAIR: Malar rash, Discoid rash, Serositis, Oral ulcer, Arthritis, Photosensitivity, Neurologic abnormality, Hematologic abnormality, ANA (positive), Immunologic abnormality, Renal involvement.

11 Describe antiphospholipid syndrome (APS)

APS is an acquired cause of hypercoagulability. Fifty percent of patients with APS have SLE. Recurrent venous and arterial thromboses and embolism are the hallmark of this syndrome. See Table 58-2.

Table 58-2 Clinical features and investigations of antiphospholipid syndrome

Clinical features Investigations

Hematologic: recurrent venous or arterial thromboses, thrombocytopenia, hemolytic anemia, renal thrombotic microangiopathy

Neurologic: stroke, transient ischemic attacks, seizures, transverse myelitis, migraines, chorea, multiinfarct dementia

Cutaneous: livedo reticularis, distal gangrene, thrombophlebitis

Pulmonary: embolism, intraalveolar hemorrhage, hypertension

Cardiac: valvular disease (vegetations), myocardial infarction

Musculoskeletal: osteonecrosis

Obstetric: recurrent miscarriages, placental insufficiency, preeclampsia, or severe eclampsia

image False-positive serologic test for syphilis: VDRL test or rapid plasma reagin

image Prolonged activated partial thromboplastin time

image Prolonged Russell viper venom time (lupus anticoagulant)

image Positive anti-cardiolipin antibody

image Positive β2 glycoprotein 1 antibody

VDRL, Venereal Disease Research Laboratory.

Catastrophic APS is a rare presentation with 50% mortality and usually is characterized by widespread small vessel thrombosis with multiorgan failure.

12 What other laboratory evaluations may be useful in the diagnosis of other connective tissue disorders?

See Table 58-3.

Table 58-3 Autoantibodies and associated disorders

Autoantibody Disorder
Rheumatoid factor RA (80%); SLE (10%); MCTD (50%-60%); Sjögren syndrome (80%-90%); infections; chronic liver and pulmonary disease and cryoglobulinemia (>40%)
Anti–cyclic citrulline peptide antibody RA
ANA profile  

image Anti-dsDNA

SLE

image Anti-Sm (Smith antigen)

SLE

image Anti-SS-A

Sjögren syndrome (70%); SLE (30%); RA; scleroderma and MCTD (rare) Anti-SS-B Sjögren syndrome (60%); SLE (15%); RA; scleroderma; MCTD (rare) Anti-RNP MCTD (95%); SLE (30%) Anti–Scl-70 Diffuse scleroderma (20%-40%) Anti-centromere Limited scleroderma (60%-90%); diffuse scleroderma (30%) Anti-histone Drug-induced lupus erythematosus Anti–Jo-1 Polymyositis Anti–neutrophilic cytoplasmic antibody Vasculitis

MCTD, Mixed connective tissue disease; RA, rheumatoid arthritis; RNP, ribonuclear protein; SLE, systemic lupus erythematosus.

13 Patients with antineutrophil cytoplasmic antibody (ANCA)–associated vasculitis frequently are seen in the intensive care unit (ICU). What diseases are associated with a positive ANCA test?

Systemic vasculitis is categorized into small, medium, and large vessel involvement. It should be considered in any patient with rapidly progressive multisystemic organ dysfunction, pulmonary-renal syndromes, or unexplained stroke or in young persons with ischemic signs, fever of unknown origin, unexplained constitutional symptoms, purpuric skin lesions, and/or mononeuritis multiplex.

There are two forms of ANCA: cytoplasmic (c-ANCA) and perinuclear (p-ANCA). If the ANCA is positive, two target antigens should also be checked: myeloperoxidase (MPO) and serine proteinase-3 (PR3). See Box 58-1.

Box 58-1 Conditions associated with positive antineutrophil cytoplasmic antibody

P-ANCA  
MPO positive: MPO negative:

Microscopic polyarteritis

Churg-Strauss vasculitis

Pauci immune glomerulonephritis

Drug-induced ANCA vasculitis(minocycline, hydralazine, propylthiouracil)

Wegener granulomatosis (10%)

Goodpasture disease

Autoimmune disease (RA, SLE, Sjögren)

Ulcerative colitis

Cystic fibrosis

Infections (HIV, subacute bacterial endocarditis, parvovirus, EBV) Malignancy

C-ANCA  
PR3 positive:  

Wegener granulomatosis (80%-90%)

Microscopic polyarteritis

Churg-Strauss vasculitis (rare)

Goodpasture disease (rare) Drug-induced ANCA vasculitis (rare)

ANCA, Antineutrophil cytoplasmic antibody; EBV, Epstein-Barr virus; MPO, myeloperoxidase; PR3, serine proteinase-3; RA, rheumatoid arthritis; SLE, systemic lupus erythematosus.

14 Diffuse alveolar hemorrhage (DAH) is a common presentation to the ICU. What are the clinical features? What are the common autoimmune conditions associated with DAH?

DAH is a catastrophic clinical syndrome caused by the accumulation of intraalveolar red blood cells from the alveolar capillaries. Patients may present with hemoptysis, anemia, radiographic findings of diffuse pulmonary infiltrates, and respiratory failure. In up to a third of cases, hemoptysis may be initially absent and patients may only describe symptoms of fever, chest pain, shortness of breath, or cough. High clinical suspicion is essential to make the diagnosis. Serial bronchoalveolar lavage is the gold standard and confirms this clinical diagnosis when lavage aliquots are progressively more hemorrhagic.

The common autoimmune diseases presenting with DAH include the following:

image ANCA-associated vasculitis: Wegener granulomatosis and microscopic polyangiitis

image SLE

image Goodpasture syndrome

image Mixed connective tissue disease

image APS

image RA

image Scleroderma

image PM

15 A patient with RA comes to the ICU with severe shortness of breath. Describe the different pulmonary causes

Pulmonary complications from RA account for 10% to 20% of all mortality.

image Parenchymal involvement: interstitial lung disease, bronchiolitis obliterans with organizing pneumonia, rheumatoid nodules

image Airway involvement: upper airway obstruction, obstructive sleep apnea, bronchiolitis (obliterative), bronchiectasis, Caplan syndrome, cricoarytenoid arthritis

image Vascular involvement: pulmonary hypertension, pulmonary vasculitis

image Pleural involvement: pleural effusion, empyema, bronchopleural fistula or pyopneumothorax, chyliform effusions, lung entrapment

image Drug-related lung toxicity: methotrexate, leflunomide, tumor necrosis factor (TNF) inhibitors, gold salts, and D-penicillamine

image Infections: pneumonia, bronchiectasis, empyema, infected nodules

Remember: Patients with RA are predisposed to atypical and fungal infections, in addition to common bacterial and viral infections. Fever and leucocytosis may be absent.

image Cardiovascular disease: pericardial effusion, myocardial infarction, angina

image Thoracic cage immobility

image Coexisting medical conditions: asthma, emphysema, congestive heart failure

16 An elderly woman comes to the ICU with fever of unknown origin, an elevated ESR, headaches, disorientation, and weakness. What rheumatologic condition should not be missed?

Giant cell arteritis (GCA) or temporal arteritis is a large-vessel vasculitis that occurs more commonly in elderly patients >50 years old and women. It can present with the following:

image Cranial symptoms: headaches, scalp tenderness, jaw claudication, diplopia, blindness, diminished temporal artery pulse, and stroke

image Polymyalgia rheumatica (PMR): gradual or acute onset of symmetric stiffness and pain in proximal muscle groups such as shoulders, hips, thighs, and neck

image Combination of PMR and cranial symptoms

image Abdominal symptoms: upper back pain, chest pain, dysphagia, dyspnea, superior vena cava syndrome due to thoracic aorta aneurysm or dissection; mesenteric ischemia

image Systemic symptoms: weight loss, fevers, fatigue, and malaise

High-dose corticosteroids (prednisone 1 mg/kg) should be started urgently to prevent visual loss from ischemic optic neuritis. ESR is usually elevated and can be helpful but if normal does not exclude GCA. A 3- to 6-cm temporal biopsy should be performed to confirm diagnosis, but steroid therapy should not be delayed while awaiting the biopsy results. The patient can still have GCA with a negative biopsy because patchy arterial involvement usually exists and therefore the right clinical context must be considered.

17 Describe important side effects of biologic agents, such as TNF-α antagonists (e.g., etanercept, infliximab, adalimumab, certolizumab, and golimumab) that should be considered in an acutely ill ICU patient

A higher occurrence of both typical and atypical infections is documented in patients taking TNF inhibitors. These include the following:

image Typical bacterial infections

image Reactivation of latent and miliary tuberculosis (TB)

image Listeriosis with symptoms of meningoencephalitis or septicemia

image Disseminated fungal diseases such as histoplasmosis and coccidioidomycosis

image Pneumocystis carinii (jirovecii) pneumonia (PCP)

image Reactivation of hepatitis B virus and herpes zoster infection

Risk factors such as occupational exposure, living in nursing homes, and living in areas where TB is endemic should be evaluated because tuberculin skin testing may be negative in immunocompromised patients.

Controversial data also exist about patients receiving biologic agents being at a higher risk for malignancy because of their immunogenic nature and demyelinating disease.

Remember: Live vaccinations should not be administered to patients taking biologic agents.

18 What adverse events associated with short- and long-term steroid use can be present in patients in the ICU?

See Box 58-2.

Box 58-2 Common acute and chronic adverse effects of glucocorticoids

Acute Chronic

image Hyperglycemia

image Hypertension

image Infections

image Behavioral changes including steroid psychosis, insomnia, and emotional instability

image Fluid retention

image Peptic ulcer disease and pancreatitis

image Impaired wound healing and ecchymoses

image Atypical presentations of community-acquired and opportunistic infections

image Osteoporosis-associated fractures occurring with minor trauma

image Osteonecrosis of large joints especially the hips, knees, ankles, and shoulders

image Proximal muscle weakness due to steroid-induced myopathy

image Higher risk of adverse cardiovascular and cerebrovascular disease

image Adrenal insufficiency

19 What precautions should be undertaken when admitting a patient taking long-term low-dose steroids to the ICU for an acute illness?

Patients taking long-term low-dose steroid therapy (prednisone >5 mg/day) for many years or taking higher doses of steroids (prednisone >20 mg) for more than several weeks may have adrenal insufficiency that may present during an acute illness or high metabolic state.

Symptoms may include fevers, severe hypotension, electrolyte disturbances, fatigue, nausea, and vomiting. Long-term steroid therapy leads to suppression of the hypothalamic-pituitary-adrenal axis. If this diagnosis is suspected, treatment with stress-dose steroids (hydrocortisone 300 mg IV in three divided doses daily) should be initiated.

20 What are the sinister signs of back pain? What causes of back pain should not be missed in a critically ill patient?

Red flags:

image Age <18 or >50 years

image Back pain >6 weeks

image History of cancer

image Unexplained weight loss, night sweats, fevers, chills

image Recent bacterial infection

image Back pain that wakes patient from sleep

image Increasing or persistent back pain despite analgesia and rest

image Immunocompromised patient or intravenous drug abuse

image Trauma

image Bowel or bladder incontinence or saddle anesthesia

image Severe or progressive neurologic deficits or motor weakness

image Prolonged corticosteroid use

A detailed history and physical examination, with emphasis on localizing the involved nerve distribution, should always be performed. In cases where this is not possible or there is suspicion of involvement, consider performing magnetic resonance imaging (MRI) or computed tomography of the spine.

Spinal epidural abscess, epidural spinal cord compression, malignancy, septic discitis, and osteomyelitis should not be missed as they could lead to neurologic deficits or death.

21 What are the causes of central nervous system (CNS) vasculitis? What specific investigations should be performed?

There are two categories of CNS vasculitis. Primary angiitis of the CNS (PACNS) is confined to the CNS without any other identifiable cause. It occurs in the fourth or fifth decade of life, in men, and rarely presents acutely. PACNS lacks systemic symptoms, and patients have normal inflammatory markers in comparison with secondary vasculitis.

Secondary CNS vasculitis usually presents with symptoms typical for the specific systemic vasculitis. Autoimmune causes include Wegener granulomatosis, Behçet disease, SLE, and, less commonly, Sjögren syndrome, RA, mixed connective tissue disease, Hashimoto thyroiditis, and multiple sclerosis.

Patients may have symptoms of severe headaches, seizures, strokelike episodes, ataxia, cognitive impairment, encephalopathy, movement disorders, and neurologic deficits.

Infections and malignancy should be ruled out. Inflammatory and autoimmune laboratory tests, lumbar puncture, MRI and angiogram, and cerebral angiogram should be performed. Leptomeningeal brain biopsy is the gold standard for diagnosis.

22 What is macrophage activation syndrome (MAS)? What investigation should be performed?

MAS is an autoimmune illness that is a form of hemophagocytic lymphohistiocytosis syndrome and is due to uncontrolled macrophage activation. It usually occurs in children or adults with autoimmune disease, especially systemic-onset juvenile idiopathic arthritis, adult-onset Still disease, or more rarely SLE.

These patients are critically ill and have fever, splenomegaly, cytopenias, hypertriglyceridemia, hypofibrinogenemia, coagulopathies, high ferritin (usually ferritin >500 mcg/L). One of the hallmarks of this disease is that they will present with decreasing cell counts and inflammatory markers. Malignancy and infection can occur concurrently or mimic MAS and therefore should be ruled out. Patients suspected to have this condition should have a bone marrow test performed, which will usually show normal or increased cellularity.

23 In the ICU, patients are seen acutely with an elevated creatine kinase (CK) level. What is the differential of an elevated CK level?

image Drug and toxin induced: statins, colchicine, ethanol, cocaine, antimalarials, corticosteroid-induced myopathy, barbiturates, zidovudine

image Infectious myositis: bacterial, viral, fungal, mycobacterial, or parasitic

image Endocrine disorders: hypothyroidism, hyperthyroidism, acromegaly, Cushing or Addison disease

image Myocardial injury

image Trauma

image Metabolic myopathies: glycogen storage or lipid metabolism disorders, electrolyte disorders

image Miscellaneous: seizures, malignant hyperthermia, motor neuron disease, rhabdomyolysis, organ failure

image Autoimmune or rheumatologic disorders: PM or dermatomyositis (DM), PMR, systemic vasculitis, sarcoidosis, inflammatory arthritides

24 What are the clinical signs and symptoms that suggest an inflammatory myopathy? What other investigations may be helpful in diagnosing an inflammatory myopathy?

In a critical setting it may be difficult to differentiate the cause of an elevated CK level. The symptoms of gradual, progressive, symmetric proximal muscle weakness or neck muscle weakness are usually suggestive of PM or PMR. In addition, if certain rashes such as a heliotrope rash, Gottron papules, shawl sign, V sign, or mechanic’s hands are present consider DM or mixed connective tissue disease.

Aldolase, aspartate transaminase, lactate dehydrogenase, and ESR may be elevated in an inflammatory myopathy. Myositis-specific autoantibodies may be present in PM and DM. An electromyogram and muscle biopsy should be performed if PM or DM is suspected. There is a 10% to 15% association with malignancy over the next 3 years in PM and DM.

Key Points Rheumatologic Emergencies in the Intensive Care Unitimage

1. An acute swollen joint indicates septic arthritis until proved otherwise. Crystal-induced arthropathy and septic arthritis can occur simultaneously in a joint.

2. Patients with severe peripheral RA are at higher risk for spinal cord compression from AAS during intubation. Beware of cricoarytenoid obstruction also occurring in these patients.

3. Prompt treatment with an ACEi should be initiated in patients with SRC.

4. Patients taking biologic medications are at a higher risk for typical bacterial infections and atypical infections such as reactivation of TB, hepatitis B, herpes zoster, PCP, listeriosis, and disseminated fungal infections.

5. In a patient in the ICU who is seen with multiorgan failure or a clinical picture resembling fulminant sepsis, consider the diagnosis of SLE or vasculitis.

Bibliography

1 Corwell B.N. The emergency department evaluation, management and treatment of back pain. Emerg Med Clin N Am. 2010;28:811–839.

2 Denton C.P., Lapadula G., Mouthon L., et al. Renal complications and scleroderma renal crisis. Rheumatology. 2009;48:iii32–iii35.

3 Hajj-Ali R.A. Primary angiitis of the central nervous system: differential diagnosis and treatment. Best Pract Res Clin Rheumatol. 2010;24:413–426.

4 Hoffman G.S., Specks U. Antineutrophil cytoplasmic antibodies (ANCA). Arthritis Rheum. 1998;41:1521–1537.

5 Jacobs J.W.G., Bijlsma J.W.J. Glucocorticoid therapy. Firestein G.S., Budd R.C., Harris E.D., et al, eds. Kelley’sTextbook of Rheumatology, 8th ed, 1. Philadelphia: Saunders, 2009;863–881.

6 Janka G. Hemophagocytic syndromes. Blood Rev. 2007;21:245–253.

7 Lara A.R., Schwarz M.I. Diffuse alveolar hemorrhage. Chest. 2010;137:1164–1171.

8 Mathews C.J., Weston V.C., Jones A., et al. Bacterial septic arthritis in adults. Lancet. 2010;375:846–855.

9 Rendt K. Inflammatory myopathies: narrowing the differential diagnosis. Cleve Clin J Med. 2001;68:505–519.

10 Ruiz-Irastorza G., Crowther M., et al. Antiphospholipid syndrome. Lancet. 2010;376:1498–1509.

11 Sorokin R. Management of the patient with rheumatic disease going to surgery. Med Clin North Am. 1993;77:453–464.

12 Tassiulas I.O., Boumpas D.T. Clinical features and treatment of systemic lupus erythematosus. Firestein G.S., Budd R.C., Harris E.D., et al, eds. Kelley’sTextbook of Rheumatology, 8th ed, 1. Philadelphia: Saunders, 2009;1263–1300.

13 Tokunaga D., Hase H., Mikami Y., et al. Atlantoaxial subluxation in different intraoperative head position in patients with rheumatoid arthritis. Anesthesiology. 2006;104:675–679.

Related posts:

Intensive Care Unit Organization, Management, and Value Status Epilepticus Bronchoscopy Skin and Soft Tissue Infections Toxic Alcohol Poisoning Hemodynamic Monitoring