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Introduction
Psychogenic Non-Epileptiform Seizures is a real disease. These events probably represent a subconscious dissociative physical response to distressing internal emotional stimuli. These attacks may look like epileptic seizures but are not truly caused by altered electrical activity in the brain but happen due to a reaction to adverse life experiences, trauma, loss or bereavement. Patients with PNES do not have a focal lesion, but rather have dysfunction that is distributed across a wide array of limbic and cortical substrates modulated by several key endocrine signals. The production of seizure-like symptoms is not under voluntary control, meaning that the person is not faking. Interestingly, about 5-20% of people with PNES also have epilepsy.

Other Terminologies

  • Pseudoseizures - Use of this particular terminology is discouraged
  • Functional Seizures
  • Dissociative Seizures
  • Non-Epileptiform Attack Disorder 

No single historical feature or combination of features is diagnostic of PNES. PNES are distinct from Epileptiform seizures as they do not show any abnormal electric discharge from the brain. The definitive test to diagnose PNES is Video EEG. Features that may suggest PNES are:
  • Same frequency but variable amplitude throughout the seizure
  • Recall of events
  • Pelvic thursting
  • Forced eye closure
  • Episodes >2min

Treatment of PNES
  1. Adequate communication and education with the patient/family
  2. Continued neurological follow-up to safely withdraw anticonvulsant medications
  3. Address comorbid psychiatric diagnoses - CBT/Antidepressants/Antipsychotics (Haloperidol/Olanzapine)

Further Reading
https://www.epilepsy.com/article/2014/3/truth-about-psychogenic-nonepileptic-seizures




Posted by:

              
     Lakshay Chanana
     
     ST4 Trainee
     Royal Infirmary of Edinburgh
     Department of Emergency Medicine
     Edinburgh
     Scotland

     @EMDidactic



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Introduction
Cellulitis is often misdiagnosed in ED. Available literature reports a misdiagnosis rate of close to 30% that leads to unnecessary admission and antibiotics. 

Cellulitis usually doesn’t affect the deeper layers of skin and presents is a poorly demarcated area of superficial bacterial infection which is painful, erythematous and warm to the touch. It is a clinical diagnosis and no labs are needed unless there are other concerns (Nec Fasc, Osteomyelitis, Abscess). Blood cultures are low yield and should be done only in critically ill and those who fail to improve. Most cases of cellulitis are due to direct inoculation and it is rare for both extremities to be affected at the same time. BILATERAL CELLULITIS IS RARE. Also, cellulitis should be painful rather than itchy. If it is chronic, it is not cellulitis.

Erythema that spreads past drawn margins does not always mean that the patient is worsening. Erythema of cellulitis can spread in the first 48 hours as a normal progression and this does NOT always indicate treatment failure. Think escalation of Antibiotics if erythema is more intense or patient is more ill-appearing or persistent fever.




Common Organisms: Streptococcus pyogenes and Staphylococcus aureas in immunocompetent, without cirrhosis, neutropenia or other risk factors. Purulence or drainage should make you think about staph and consider MRSA in purulent cellulitis if there are risk factors associated. Penicillins or first-generation cephalosporin is a good first choice. Options for MRDA include Sulfamethoxazole/trimethoprim, linezolid, and doxycycline.

(Broad-spectrum antibiotics should be used in critically ill, high risk fo uncommon organismsHigh risk for resistant bacteria)


Mimics
  • DVT - Usually differentiable on history and exam
  • Stasis Dermatitis - Usually bilateral but can be unilateral as well. Usually due to underlying bilateral venous insufficiency. Leaked out fluid irritates the skin and causes redness. It may be acute (appears and feels as bilateral cellulitis) or chronic (thick hyperpigmented skin with hemosiderin deposits).
  • Lipodermatosclerosis. This looks like erysipelas and commonly seen in patients with chronic venous insufficiency. It tends to occur on the medial aspect of the ankle. This can be treated with low dose steroids.
  • Necrotising Fasciitis - Pain out of proportion of exam and pain extending beyond the borders of erythema. Most patients are ill-looking with unstable vital signs. Other possible features are insensate skin overlying the area of infection, “Dishwater-appearing fluid” drainage from within the wound. Erythema will often progress rapidly, even within hours. Admit for observation if any concerns for NF. 
  • Contact dermatitis presents with pruritis which is a response to an external exposure seen the site of the exposure.
  • Dermatohypersensitivity reaction. Allergic-type reaction due to bites, viral infections, medications. 
  • Lymphedema, gout and erythema migrans. Usually differentiated based on history
  • Calciphylaxis - This is a painful, relapsing and remitting condition which is often seen in cases ofunderlyingg renal failure, diabetes, obesity, liver disease or are taking warfarin. Calcium deposition in blood vessels of the dermis causes skin necrosis and lead to eschars over adipose areas. 


Venous stasis and lymphedema predisposes to cellulitis. 
If on elevating the legs for 1-2 mins, erythema goes away then it is less likely to be cellulitis


Oral v/s IV Antibiotics for Cellulitis
There is good evidence that oral antibiotics are just as good across a wide range of con- ditions such as cellulitis, pneumonia, pyelonephritis, osteomyelitis and even endocarditis. Majority of patients with uncomplicated cellulitis do well with oral antibiotics. 


Take Home
  • Think about alternative diagnoses for erythema and warmth
  • Bilateral lower extremity cellulitis is rare
  • If on elevating the legs for 1-2 mins, erythema goes away then it is less likely to be cellulitis
  • When discharging on oral antibiotics, review high risk patients in 48-72 hours 


References:
  • Raff AB, Kroshinsky D. Cellulitis: a review. JAMA. 2016; 316(3): 325-37.
  • McCreary EK, Heim ME, Schulz LT, et al. Top 10 myths regarding diagnosis and treatment of cellulitis. J Emerg Med. 2017 Oct; 53(4): 485-492.
  • Aboltins, CA et al. Oral versus parenteral antimicrobials for the treatment of cellulitis: a randomized non-inferiority trial. J Antimicrob Chemother. 2015 Feb;70(2):581-6.
    PMID: 25336165



    Posted by:

                  
         Lakshay Chanana
         
         ST4 Trainee
         Royal Infirmary of Edinburgh
         Department of Emergency Medicine
         Edinburgh
         Scotland

         @EMDidactic


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Introduction
Proximal femur fractures are a common injury, particularly in the elderly. If seen in the younger population then it signifies significant degree of forces involved. Fractures can be described as intracapsular (NOF) or extracapsualar (intertrochanteric, transtrochanteric and subtrochanteric). Intracapsular fractures are at high risk of non-union and avascular necrosis due to compromisedd blood supply and often arthroplasty (either hemiarthroplasty or total hip replacement) may be indicated for these fractures. It is important to always consider the possibility of a pathological fracture in any patient who has a known diagnosis of malignancy. 



Intracapsular - Commonly referred to as NOF. Typically seen in elderly patients who present with trivial trauma, such as a fall from standing height. They patints often have osteoporosis or a lytic lesion. Neck of femur fractures are classified into 4 grades according to the Garden system based on an increasing degree of displacement. 



The management of intracapsular fracture depends on the degree of displacement and to a degree the fitness of the patient. Undisplaced fractures are fixed (cannulated hip screws) and displaced fractures are replaced, usually with a hemiarthroplasty. 

Exceptions - Displaced fractures in fit young patients should be fixed within 6 hours rather than replaced because there is a high risk of avascular necrosis, to insert a joint replacement in younger patients is the last resort as it will almost certainly need multiple revision surgeries as the total hip replacement wears out. healthy patients between the ages of 40 and 60 would do poorly with a hemiarthroplasty as they still have a high functional demand. These patients should be treated with a total hip replacement which has much better functional outcomes. 

Intertrochanteric - Extracapsular injuries and thus pose little concerns to the blood supply of the femoral head. Treatment is fixation rather than replacement. Generally fixed with a compression hip screw. 

Subtrochanteric - Extracapsular fractures typically seen in two circumstances ie. high energy trauma and due to lytic lesions. Occasionally also seen as fragility fractures in the elderly. Fixation is the treatment of choice and intramedullary nail with a hip screw is typically used.


ED Management
  • Pain Relief - Low dose opioids/FICB
  • Bloods and CXR - Preop
  • IV Fluids
  • Look for concomitant injuries  and other acute medical problems 
  • Ortho Referral




Posted by:


              
     Lakshay Chanana
     
     ST4 Trainee
     Royal Infirmary of Edinburgh
     Department of Emergency Medicine
     Edinburgh
     Scotland

     @EMDidactic




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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


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      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

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        Why do Emergency Medicine?

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


        Why Do Emergency Medicine - YouTube


        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
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        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
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        MedReach is an online video-learning platform for health professionals with two broad aims:
        1. To provide fair and equal access to world-leading medical education for all health care professionals;
        2. To improve healthcare learning and delivery in low-income countries.
        Access to high-quality learning is currently limited by time, funding and geographic location with those in remoter communities and low-income countries the most disadvantaged. MedReach aims to overcome these barriers by filming high-impact courses and conferences, and providing online access at a time, pace and location that suits the user. We charge a modest amount to those that can afford it (high-income countries) and give it all for free to health-professionals in low-income countries, as well as donating a significant portion of sales to healthcare projects in poorly resourced areas.
        So, learn from ‘world-experts’, take notes, export course certificates and summaries of learning, and at the same time contribute to healthcare improvement in areas that need support.


        We often hear about educational courses, but travelling to another country and the heavy costs involved to attend an 6-8hr course is always a setback.  Having done a few of MedReach courses personally, this is something I highly recommend for Emergency Medicine and other acute care specialities trainees. Watching eminent educators such as Rich Levitan and Arun Sayal and learning from them at our own pace and comfort is a joy. To begin with, I was a bit skeptical about learning skills requiring some dexterity with a video-based course but achieving finesse is certainly possible if your basics are set right. 

        Do check out https://www.medreach.org/courses/ for more information. 



        Posted by:

                      
             Lakshay Chanana
             
             ST4 Trainee
             Royal Infirmary of Edinburgh
             Department of Emergency Medicine
             Edinburgh
             Scotland

             @EMDidactic




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        What is BPD?
        BPD is a type of ‘personality disorder’ in which people struggle with emotions ultimately affecting their relationships with others. It is also called as Emotionally Unstable Personality Disorder (EUPD). It is believed that BPD results from traumatic childhood experiences (neglect or being abandoned, physical, emotional or sexual abuse). People with BPD may experience:
        • feeling isolated/ abandoned 
        • self-harm or suicidal thoughts
        • difficulty coping with stress
        • strong emotions 
        • misusing alcohol and prescription drugs
        • Using illegal drugs and substances
        • Understanding others points of view
        • Being able to maintain a home

        People with BPD typically have at least five of the symptoms below:
        • Feeling worried about people abandoning you, and would do anything to stop that happening
        • Feeling intense emotions that last from a few hours to a few days and can change quickly (for example, from feeling very happy and confident to suddenly feeling low and sad)
        • Having a strong sense of who you are, and it can change significantly depending on who you're with
        • Finding hard to make and keep stable relationships
        • Feeling empty a lot of the time
        • Acting impulsively and do things that could harm you (such as binge eating, using drugs or driving dangerously)
        • You often have feeling of self-harm
        • Having intense feelings of anger, which are really difficult to control
        • Feeling paranoia or dissociation

        Types of EUPD


        • Borderline- More difficulties with relationships, self-harming and feelings of emptiness.
        • Impulsive- Issues with impulsive behaviour and angry feelings.



        Treatment for BPD


        1) Dialectical Behaviour Therapy (DBT)
        DBT helps to build skills to deal with distress. DBT can help to learn how to control harmful ways of coping with distress, such as self- harming or using drugs or alcohol. DBT usually involves weekly individual and group sessions.

        2) Mentalisation-Based-Therapy (MBT)
        MBT helps people who make assumptions about what other people think or feel. The goal of MBT is to improve your ability to recognise your own and others' mental states, learn to "step back" from your thoughts and examine them to see if they're valid. MBT is based on the concept that people with BPD have a poor capacity to mentalise. Mentalisation is the ability to think about thinking. 

        3) Cognitive Behavioural Therapy (CBT) – Aims to help understand how thoughts and beliefs might affect feelings and behaviour.

        4) Cognitive Analytic Therapy (CAT) – Combines CBT's practical methods with a focus on the relationship between the patient and therapist. 

        5) Other talking therapies – such as schema-focused cognitive therapy, psychodynamic therapy, interpersonal therapy or arts therapies.


        ED visits and typical presentations

        • Self-harm - Do Risk Assessmnet and manage overdoses based on the type of drug taken
        • Drugs and alcohol - Observe, give time to sober up and re-assess
        • Impulsive behaviours (driving erratically, having more sexual partners, and spending money without thinking)
        Emergency Medicine Physicians should adopt a calm and non-threatening attitude towards this group of patients. With no rapport, it can be challenging dealing with these sensitive induviduals in the midst of a chaotic ED. People with BPD often find that simply talking to somebody who understands their condition can help bring them out of a crisis. It becomes critical to step back and try to understand the crisis from the person’s point of view and explore their concerns. Use empathetic and open questioning including validating statements. Being a good listener and listening without interrupting goes a long way in such situations. If you come across a frequent attender, then check their anticipatory care plan on records. 

        Prior to dishcarge, ensure they have helpline contact details before discharge (Mental Health Nurse, Social Worker) and in case of a severe crisis when behaviour poses a significant risk, discuss with MH team for admission or detention. No medication is currently licensed to treat BPD but medications are often used if you have another associated mental health condition, such as Anxiety/Depression. 



        Posted by:


                      
             Lakshay Chanana
             
             ST4 Trainee
             Royal Infirmary of Edinburgh
             Department of Emergency Medicine
             Edinburgh
             Scotland

             @EMDidactic



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        Introduction
        Pain is one the most common presentation to the emergency department (ED) and therefore, we should be aware of novel treatments options, adjuncts that can be used in addition to conventional therapies. Opioids are among the most commonly used analgesics in ED. Recently, a lot has been written about Low Dose Ketamine or Sub-Dissociative doses  (SDK) of ketamine to treat intractable pain or as a part of multimodal approach. 

        Classically, ketamine has been used as an anesthetic agent for procedural sedation or intubation but low dose or sub- dissociative dose ketamine (SDK) may be used as an adjunct to opioids or as a single agent. SDK dosing is anywhere from 0.1-0.3 mg/kg where ketamine acts not as an anesthetic, but rather as an analgesic. Generally,  SDK does not produce many of the potentially adverse respiratory or hemodynamic effects of other analgesics, and may be used as a safe and effective alternative or adjunct to opioids. Ketamine is both hydrophilic and lipophilic which allows administration via various routes. 

        It has been found that SDK lowers pain scores and has functionally equivalent efficacy to morphine for short-term analgesia in the ED. WHen used with opioids, SDK also reduces the overall dose of opioid analgesics and the need for re-dosing. 

        Mechanism of action - Ketamine
        After cell injury, the NMDA/glutamate receptor complex is activated in the dorsal horn of the spinal cord and these receptors are pivotal in developing hyperalgesia, allodynia and ultimately, central sensitization and wind up phenomenon (Wind-up is a frequency-dependent excitability of neurons in the dorsal horn of the spinal cord and the activation of the NMDA/glutamate receptor complex is a necessary step in the development of the wind-up phenomenon), which leads to the development of persistent and neuropathic pain as well as opioid-tolerant pain. SDK non-competitively blocks the NMDA receptors with its antihyperalgesic, antiallodynic and anti-tolerance effects. This mechanism of action of ketamine is responsible for its utility in managing a variety of acute and chronic (neuropathic, malignant, opioid-tolerant, opioid-induced hyperalgesic states) painful conditions as an adjuvant analgesic or single agent.
        Ketamine undergoes extensive hepatic metabolism (via cytochrome P450 enzymes) with norketamine being an active metabolite with 1/3 of the potency of ketamine. Ninety percent of the drug is excreted in urine in the form of metabolites with 2-4% of the drug remains unchanged
        In theory, patients with severe liver and renal dysfunction may have prolonged clearance and accumulation but there is no data to imply that SDK is unsafe in patients with liver or renal dysfunction

        SDK Dosing:

        0.1-0.3mg/kg over 15 minutes diluted in 100ml NS for short infusion - No monitoring necessary
        0.15-0.2mg/kg/hr (continuous infusion): 100mg Ketamine in 100ml NS, IV pump is
        necessary, titrate q30 min by 5mg until the pain is optimized or develop psycho-perceptual effects, monitoring is preferred
        • Analgesic dose (0.1-0.3 mg/kg) - At these low doses, ketamine has minimal psycho-perceptual effects and works as a strong analgesic. Typically, these doses do not require monitoring.
        • Recreational dose (0.2-0.5 mg/kg) ketamine works as a great analgesic but also leads to distortions of perception. 
        • Dissociative dose (>0.7 mg/kg) ketamine - These doses keep them awake but unconscious. Typically this range of dose is used for PSA or intubation. 

        Sitiations where SDK can be used:
        Acute traumatic and non-traumatic pain
        Complex regional pain syndrome
        Functional abdominal pain
        Migraine headache
        Neuropathic and radicular pain
        Sickle cell crisis
        Chronic pain syndromes. 

        Note: SDK does not cause respiratory depression or increase in intra-cranial or intra-ocular pressure. 

        Side effects (directly related to speed of administration):
        Nausea/Vomiting, Dizziness, Lightheadedness, Feeling of unreality, dysphoria
        Emergence reactions - Not seen at low doses


        Indications
        • Acute pain: traumatic, non-traumatic, brief painful procedures, post-operative pain
        • Chronic: central pain (post stroke pain), phantom pain, neuropathic pain, cancer pain
        • Opioid-tolerant pain
        • Opioid-induced hyperalgesic states

        Contraindications
        • Allergy to ketamine
        • Age <2 months
        • History of schizophrenia


        Take Home
        SDK used alone or in combination with opioids is safe and effective for the treatment of acute pain in the ED and may result in opioid sparing. Its use has been associated with relatively high rates of minor and short lived adverse side effects that can be reduced by utilizing a short-infusion of ketamine via IV of 0.3 mg/kg over 15 min.


        References:
        1. Johansson P, Kongstad P, Johansson A. The effect of combined treatment with morphine sulphate and low-dose ketamine in a prehospital settingScand J Trauma Resusc Emerg Med. 2009 Nov 27;17:61.
        2. Galinski M, Dolveck F, et al. Management of severe acute pain in emergencysettings: ketamine reduces morphine consumption. Am J Emerg Med. 2007 May;25(4):385- 90
        3. Ahern TL, Herring AA, Anderson ES, Madia VA, et al. The first 500: initial experience with widespread use of low-dose ketamine for acute pain management in the ED. Am J Emerg Med. 2015 Feb;33(2):197-201
        4. Miller JP, Schauer SG, Ganem VJ, Bebarta VSLow-dose ketamine vs morphine for acute pain in the ED: a randomized controlled trial Am J Emerg Med. 2015 Mar;33(3):402-8
        5. Motov S, Rockoff B, Cohen V, Pushkar I, et al. Intravenous Subdissociative-Dose Ketamine Versus Morphine for Analgesia in the Emergency Department: A Randomized Controlled Trial. Ann Emerg Med. 2015 Mar;22(3):251-7
        6. Goltser A, Soleyman-Zomalan E, Kresch F, Motov S. Short (low-dose) ketamine infusion for managing acute pain in the ED: case-report series. Am J Emerg Med. 2015 Apr;33(4):601.e5-7.
        7. Ahern TL, Herring AA, Miller S, Frazee BW. Low-Dose Ketamine Infusion for Emergency Department Patients with Severe Pain. Pain Med. 2015 Jul;16(7):1402-9.
        8. Yeaman F, Meek R, Egerton-Warburton D, Rosengarten P, et al. Sub-dissociative-dose intranasal ketamine for moderate to severe pain in adult emergency department patients. Emerg Med Australas. 2014 Jun;26(3):237-42
        9. Motov S, Mai M, Pushkar I, Likourezos A, et al. A prospective randomized, double-dummy trial comparing IV push low dose ketamine to short infusion of low dose ketamine for treatment of pain in the ED. Am J Emerg Med. 2017 Aug;35(8):1095-1100. doi: 10.1016/j.ajem.2017.03.004. Epub 2017 Mar 3.


        Posted by:


                      
             Lakshay Chanana
             
             ST4 Trainee
             Royal Infirmary of Edinburgh
             Department of Emergency Medicine
             Edinburgh
             Scotland

             @EMDidactic



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