Septic Arthritis

Septic arthritis is a destructive disease process classically presenting as a red, hot and swollen joint. The disease has a bimodal incidence, which peaks in young children and adults over age 55 years. Unfortunately, septic arthritis is not always easy to diagnose and  presentations may be subtle without classical signs, symptoms, or laboratory markers. It remains one of those cannot miss diagnosis which are always fraught with fear. Therefore, the dictum is "Red Hot Swollen joints should be tapped" to r/o Septic Joint.   Fluid is then sent for Gram Stain, C/S, White Cell count and Differential count, and Crystal analysis. 

Routes of Spread: Common routes of spread is hematogenous followed by direct inoculation (trauma or localised spread from a surrounding soft tissue infection)

Common Joints - Knee>Hip>Shoulder>Elbow


Risk Factors for Septic Arthritis (More abnormal joint, more likely Septic Arthritis)

• Bacteremia/systemic infection
• IVDU (may have sternoclavicular and sternomanubrial joint involvement)
• Overlying skin infection
• Diabetes Mellitus
• Arthritic Joints, Prosthetic joints
• Elderly, Immunocompromised states
• Recent joint surgery or procedure

Common Organisms

• Staph Aures 40%
• Streptocossus 30%
• GNB 20%
• Gonococcal arthritis - Most common cause of septic arthritis in the sexually active patient population. Presents as migratory polyarthritis and may involve several joints (wrist, knee and ankles), or include a rash/tenosynovitis. 4:1 female to male predominance.

Clinical Presentation (No combination of exam findings can definitively diagnose septic arthritis)

• Typical - Swollen, Red, Immobile and Tender joint
• Pain is present in about 80%. Joint tenderness has sensitivity approaching 100%
• Fever is seen only in about 50% 
• Generalized tenderness with painful limitation of active and passive range of motion. Focal tenderness and pain limited to specific movements on an active range of motion testing is more typical of periarticular inflammation (skin, bursa, tendons).

Immunocompromised patients often have polyarticular involvement and present atypically. Sudden onset of pain is more suggestive of intrinsic joint pathology, such as septic arthritis.

Work up (Serum blood tests do not rule out septic arthritis)

• Synovial Fluid Analysis - Synovial fluid with a WBC count > 50,000/mm with a polymorphonuclear cell count > 90%. However, in culture-proven septic arthritis, this WBC count is reached only in 50 – 75% of cases. Therefore, lower WBC counts cannot exclude the presence of septic arthritis. A synovial fluid WBC count >100,000/mm is more specific. MRSA-associated septic arthritis (leading cause in prosthetic joints) may have lower synovial fluid WBC counts only up to 15,000 cells/μL
• Use CRP/ESR/WCC with caution - Normal levels cannot rule out septic arthritis
• Positive Gram stain can be diagnostic; however, a negative result for bacteria cannot rule out septic arthritis (sensitivity only 50-60%). Culture remains the most sensitive test (>90%).
• Presence of crystals shouldnot be used to rule out septic arthritis. Gout and Septic Arthritis can co-exist in the same joint. 

Synovial lactate has the best diagnostic accuracy in septic arthritis, based on several studies. Levels above 10 mmol/L demonstrate +LRs ranging from 20 to infinity

Imaging tests offer little assistance in the diagnosis of septic arthritis. Radiographs may demonstrate effusion or soft tissue swelling. Computed tomography (CT) has greater sensitivity for effusions and edema but is unreliable early in the disease course to evaluate for septic arthritis. Ultrasound (US) can be used to localize joint swelling and target the site for optimal aspiration. 

Management

• Analgesia
• Joint aspiration
• Empiric Antibiotics (should provide gram-positive and gram-negative coverage)
• Orthopedic Referral consultation

Take Home

• More abnormal joint, more likely Septic Arthritis
• Immunocompromised patients often have polyarticular involvement and present atypically. 
• Sudden onset of pain is more suggestive of intrinsic joint pathology, such as septic arthritis.
• Serum blood tests do not rule out septic arthritis
• If suspicion is still high after equivocal or dry tap, admit the patient and initiate empiric IV antibiotics while the synovial culture results

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh

     Department of Emergency Medicine

     Edinburgh

     Scotland

     @EMDidactic

Myths in Diagnosis of ACS

Myth 1

Absence of Classic Chest Pain obviates the need for ACS work up

The absence of chest pain in no way excludes the diagnosis of ACS. Around 33-50% of the patients with ACS present to the hospital without chest pain. Close to 20% of patients diagnosed with acute MI present with symptoms other than chest pain. Risk factors associated with the absence of chest pain included age, female gender, non-white race, diabetes mellitus, and a prior history of congestive heart failure or stroke. Over the age of 85, 60–70% of patients with acute MI present without chest pain; shortness of breath is the most frequent anginal equivalent in this population.

Patients experiencing an acute MI without chest pain are more likely to suffer delays in their care. They were also more likely to die in the hospital compared to patients who presented with chest pain. Over the age of 85, 60–70% of patients with acute MI present without chest pain.


Myth 2

Reproducible chest wall tenderness on palpation rules out ACS

The combination of three variables – sharp or stabbing pain, no history of angina or acute MI, and pain that was pleuritic, positional, or reproducible – is considered as a very low-risk group. Chest pain localized to a small area of the chest is often thought to suggest a musculoskeletal etiology. In one study, however, 27 of 403 patients (7%) with acute MI localized their pain to an area as small as a coin. On examining the patient, one should be careful in determining if the pain induced by chest palpation is the same pain as the presenting pain and more importantly think if the history is congruent with MSK pain. If there is no defined injury or event that could have led to a soft tissue injury, we should be reluctant to render a diagnosis of musculoskeletal pain.

Several studies have shown that chest wall tenderness can be misleading. Although certain chest pain characteristics decrease the likelihood of acute MI, none is powerful enough to support discharging at-risk patients without additional testing. In patients with chest pain, chest wall tenderness may suggest that acute MI is less likely but it does not effectively rule out the diagnosis. Given the potential implications of missing ACS, using chest wall tenderness as an independent rule out strategy is not recommended in patients at risk for ACS.

Myth 3
A normal ECG and normal cardiac enzymes rule out ACS

No historical complaint, physical finding, or ECG pattern has a negative predictive value of 100% for MI. Rather the correct statement would be this - Patient is less likely to be experiencing an MI if the ECG is normal, but further work up is needed to discard the diagnosis. Use ECG as more of a rule-in test, not a rule-out test. 

Cardiac markers provide a non-invasive means of determining whether myocardial damage has occurred. When ischemia gives way to infarction, the myocardial cell membrane is disrupted and various chemical markers are released into the systemic circulation. 
Cardiac Troponins  (I or T) are now the preferred cardiac markers for identifying myocardial damage. It is important to remember that troponin can only detect myocardial cell death but not ischemia.


Take Home:

• Do not exclude the diagnosis of acute cardiac ischemia or MI based on the absence of pain, especially when evaluating dia- betic patients, the elderly, and women.
• Never use reproducible chest wall tenderness to exclude the diagnosis of acute MI.
• Neither a single normal ECG nor a single negative set of cardiac enzymes should be used to rule out acute cardiac schema. 

References:

1. Canto JG, Shlipak MG, Rogers WJ, et al. Prevalence, clinical characteristics, and mortality among patients with myocardial infarction presenting without chest pain. J Am Med Assoc 2000; 283:3223–9.
2. 2. Dorsch MF, Lawrence RA, Sapsford RJ, et al. Poor prognosis of patients presenting with symptomatic myocardial infarction but without chest pain. Heart 2001; 86:494–8.
3. Gupta M, Tabas JA, Kohn MA. Presenting complaint among patients with myocardial infarction who present to an urban, public hospital emergency department. Ann Emerg Med 2002; 40:180–6.
4. Uretsky BF, Farquahr DS, Berezin AF, et al. Symptomatic myocardial infarction without chest pain: prevalence and clini- cal course. Am J Cardiol 1977; 40:498–503.
5. Bayer AJ, Chadha JS, Farag RR, et al. Changing presentation of myocardial infarction with increasing old age. J Am Geriatr Soc 1986; 34:263–6.
6. Lee TH, Cook EF, Weisberg MC, et al. Acute chest pain in the emergency room. Identification and examination of low risk patients. Arch Intern Med 1985; 145:85–9.
7. Lee TH, Rouan GW, Weisberg MC, et al. Clinical characteristics and natural history of patients with acute myocardial infarction sent home from the emergency room. Am J Cardiol 1987; 60:219–24.
8. Solomon CG, Lee TH, Cook EF, et al. Comparison of clinical presentation of acute myocardial infarction in patients older than 65 years of age to younger patients: the Multicenter Chest Pain Study experience. Am J Cardiol 1989; 63:772–6.
9. Swap CJ, Nagurney JT. Value and limitations of chest pain his- tory in the evaluation of patients with suspected acute coronary syndromes. J Am Med Assoc 2005; 294:2623–9. 

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh

     Department of Emergency Medicine

     Edinburgh

     Scotland

     @EMDidactic

Why do Emergency Medicine

Why do Emergency Medicine?

Listen from the inspirational team of emergency healthcare providers in Edinburgh. 

For more, checkout EdinburghEM website 

Initially published by RCEM youtube channel - 21/01/2016

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh

     Department of Emergency Medicine

     Edinburgh

     Scotland

     @EMDidactic

Gullian Barre Syndrome

Guillain-Barré syndrome (GBS) is a heterogeneous group of immune-mediated peripheral neuropathies which presents as evolving polyradiculoneuropathy preceded by a triggering event (often an infection). Cross-reactivity between the pathogen and the nerve tissue sets up the autoimmune response. It typically manifests as a symmetric motor paralysis with or without sensory and autonomic disturbances. The progressive phase of this syndrome is followed by a plateau phase of persistent, unchanging symptoms. Improvement begins within days of the plateau and the time to resolution of symptoms varies among patients.

Patients commonly report a respiratory tract infection or gastroenteritis that resolved when the neuropathy began. Campylobacteriosis is the most common precipitant in GBS.  Other antecedent infections include cytomegalovirus, HIV, Epstein-Barr virus, and varicella-zoster virus.

Typical Presentation

• Weakness (Proximal>Distal, Legs>Arms) accompanied by tingling dysesthesias in the extremities 
• Areflexia few days of symptom onset.
• Cranial nerve involvement may affect airway maintenance, facial muscles, eye move- ments, and swallowing. 
• Shoulder, Back, Thigh Pain (severe, occurring with even the slightest of movements)

The patient with Guillain-Barré syndrome typically presents with weakness accompanied by tingling dysesthesias in the extremities.

Types of GBS
GBS has five distinct subtypes which can be distinguished electrodiagnostically and pathologically. 

1. Acute inflammatory demyelinating polyradiculoneuropathy (AIDP)

• Autoimmune disorder, antibody mediated
• Triggered by antecedent viral or bacterial infection Electrophysiologic findings demonstrate demyelination. Inflammatory demyelination may be accompanied by axonal
• nerve loss.
• Remyelination occurs after the immune reaction stops.

2. Acute motor axonal neuropathy (AMAN)

• Pure motor axonal form of neuropathy 
• 2/3rd of patients are seropositive for campylobacteriosis.
• Electrophysiologic studies are normal in sensory nerves
• Reduced or absent in motor nerves. 
• Recovery is typically more rapid. High proportion of pediatric patients

3. Acute motor sensory axonal neuropathy (AMSAN)

• Wallerian-like degeneration of myelinated motor and sensory fibers 
• Minimal inflammation and demyelination
• Similar to AMAN except AMSAN affects sensory nerves and roots 
• Typically affects adults

4. Miller Fisher syndrome

• Rare disorder
• Rapidly evolving ataxia, areflexia, mild limb weakness, and ophthalmoplegia
• Sensory loss unusual, but proprioception may be impaired. Demyelination and inflammation of cranial nerve III and VI, spinal ganglia, and peripheral nerves
• Reduced or absent sensory nerve action potentials, tibial H reflex is usually absent.
• Resolution occurs in one to three months.

5. Acute panautonomic neuropathy

• Rarest of all the variants
• Sympathetic, parasympathetic nervous systems are involved. Cardiovascular involvement is common (postural hypotension, tachycardia, hypertension, dysrhythmias). 
• Blurry vision, dry eyes, anhidrosis, gastrointestinal pseudo-obstruction, and urinary retention 
• Recovery is gradual and often incomplete. 
• Often combined with sensory features

Diagnosis
GBS is the most common type of rapidly evolving, generalized peripheral nervous system disorder. However, there are several mimics that must be considered.

Diagnostic Criteria for Typical Guillain-Barré Syndrome Features required for diagnosis

• Progressive weakness in both arms and legs Areflexia

Features strongly supporting the diagnosis

• Progression of symptoms over days, up to four weeks
• Relative symmetry of symptoms
• Mild sensory symptoms or signs
• Cranial nerve involvement, especially bilateral weakness of facial muscles
• Recovery beginning two to four weeks after progression ceases 
• Autonomic dysfunction
• Absence of fever at onset
• High concentration of protein in cerebrospinal fluid, with fewer than 10 cells per cubic millimeter 
• Typical electrodiagnostic features

Features excluding diagnosis

• Diagnosis of botulism, myasthenia, poliomyelitis, or toxic neuropathy Abnormal porphyrin metabolism
• Recent diphtheria
• Purely sensory syndrome, without weakness

Differential Diagnosis Guillain-Barré Syndrome

• Basilar artery occlusion (asymmetric limb paresis)
• Botulism (descending paralysis)
• Heavy metal intoxication (confusion, psychosis, organic brain syndrome)
• Hypophosphatemia (irritable, apprehensive, hyperventilation, normal cerebrospinal fluid)
• Metabolic myopathies (cerebral and cerebellar symptoms) 
• Myasthenia gravis (weakness and fatigue that improves with rest) 
• Neoplastic meningitis (asymmetric spastic paralysis)
• Neurotoxic fish poisoning (spontaneous recovery within 24 hours) 
• Paraneoplastic neuropathy (chronic)
• Poliomyelitis (purely motor disorder with meningitis)
• Polymyositis (chronic, affects proximal limb muscles)
• Spinal cord compression (asymmetric)
• Tick paralysis (sensory changes absent, normal cerebrospinal fluid) 
• Transverse myelitis (abrupt bilateral leg weakness, ascending, sensory)
• Vasculitic neuropathies (mononeuropathy)

The diagnosis of GBS is based on typical clinical features, electrodiagnostic examination and examination of the cerebrospinal fluid (CSF) can aid in the diagnosis. Characteristic CSF findings consist of elevated protein without pleocytosis (abnormal number of cells in the CSF). 

Treatment
1. Supportive care (Analgesia, Fluids/Electrolytes, Physical Therapy, Nutrition, DVT Prophylaxis, Ventilation)
2. Specific therapy (IVIg, Plasmapheresis)

If patients advance past the acute phase of illness, most will recover function. However, the neuropathy can advance so rapidly that endotracheal intubation and mechanical ventilation may be necessary within 24 hours of symptom onset. Therefore, all patients who have GBS should be admitted to a hospital for close observation for respiratory compromise, cranial nerve dysfunction, and autonomic instability. 

Indications to Consider Intubation

• Forced vital capacity <20 mL per kg
• Maximal inspiratory pressure <30 cm H2O
• Maximal expiratory pressure <40 cm H2O
• Progression is noted with a reduction of more than 30 per cent in vital capacity, maximal inspiratory pressure, or maximal expiratory pressure

Other predictors of subsequent mechanical ventilation:
(1) time from GBS onset to hospital admission of less than seven days
(2) inability to lift the elbows or head above the bed
(3) inability to stand
(4) ineffective coughing
(5) increased liver enzyme levels

Specific treatment should be initiated soon after diagnosis. High-dose intravenous immunoglobulin (IVIg; 400 mg per kg daily for five days) or plasmapheresis can be initiated. IVIg and plasmapheresis are considered as equally effective therapies. 

Disadvantages of plasmapheresis include its rare complications, such as sepsis, that are believed to be caused by depletion of immunoglobulins. If fresh frozen plasma is used as replacement fluid, there is a risk of acquiring viral infections such as hepatitis and HIV. IVIg treatment has advantages over plasmapheresis because it is easier to administer, has significantly fewer complications, and is more comfortable for the patient. 

Despite its benefits, there are side effects from this IVIg therapy such as congestive heart failure and renal insufficiency. Patients may develop fever, myalgia, headache, nausea, and vomiting, but these “influenza-like” symptoms are self-limiting. A history of previous anaphylaxis to IVIg is a contraindication to repeat treatment. 

Corticosteroids were once believed to be useful in the treatment of GBS because of its immune-mediated inflammatory mechanism. However, a Cochrane Database Review of randomized trials, which included 195 patients treated with corticosteroids compared with controls, showed no difference in the outcome. Corticosteroids no longer have a role in GBS treatment.

Approximately 85 per cent of patients with GBS achieve a full and functional recovery within six to 12 months. 

Take Home:

• Guillain-Barré syndrome (GBS) is a heterogeneous group of immune-mediated peripheral neuropathies which presents as evolving polyradiculoneuropathy. It typically presents as Ascending Symmetrical Weakness (Proximal>Distal, Legs>Arms) accompanied by tingling dysesthesias in the extremities, Areflexia, Cranial nerve lesions and Shoulder, Back, Thigh Pain 
• Patients commonly report a respiratory tract infection or gastroenteritis that resolved when the neuropathy began. Campylobacteriosis is the most common precipitant in GBS.  
• Therefore, all patients who have GBS should be admitted to a hospital for close observation for respiratory compromise, cranial nerve dysfunction, and autonomic instability. 
• Treatment of GBS includes Supportive care (Analgesia, Fluids/Electrolytes, Physical Therapy, Nutrition, DVT Prophylaxis, Ventilation) and Specific therapy (IVIg, Plasmapheresis)

References:

• Lindenbaum Y, Kissel JT, Mendell JR. Treatment approaches for Guillain-Barré syndrome and chronic inflammatory demyelinating polyradiculoneuropathy. Neuro Clin 2001;19:187-204.
• Hughes RA, Wijdicks EF, Barohn R, Benson E, Cornblath DR, Hahn AF, et al. Practice parameter: immunotherapy for Guillain-Barré syndrome: report of the Quality Standards Subcommittee of the American Academy of Neurology. Neurology 2003;61:736-40.

• Hughes RA, van Der Meche FGA. Corticosteroids for treating Guil- lain-Barré syndrome. Cochrane Database Syst Rev 2003;(4): CD001446. Review.
• Zochodne DW. Autonomic involvement in Guillain-Barré syndrome: a review. Muscle Nerve 1994;17:1145-55
• Newswanger DL, Warren CR. Guillain-Barré syndrome. American family physician. 2004 May 15;69(10).

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh

     Department of Emergency Medicine

     Edinburgh

     Scotland

     @EMDidactic