Things I learned this week - Paediatrics 1

1. Headache in Children

2. Using Paracetamol as an Anti-emetic

3. Croup - Clinically relevant classification from PedsEM Morsels

4. Diagnosing and Treating Constipation in Children

5. Fever phobia RANT

Posted by:

              

     Lakshay Chanana

     Emergency Medicine Trainee

     South East Scotland Deanery
     Edinburgh

     @EMDidactic

Extensor Mechanism Injuries

The extensor mechanism comprises of the quadriceps muscles and tendon, medial and lateral retinacula, patella, patellar tendon, and tibial tubercle. Tendons of the extensor mechanism are extremely resistant to tensile loads and do not rupture under normal physiologic conditions, even with significant degrees of stress. Injury generally happens due to sudden vigorous contraction of the muscle with the knee in a flexed position, laceration, or a direct impact. Disruption may occur at any level from the quadriceps muscle to the insertion on the tibial tubercle. 

Rupture of the quadriceps tendon usually occurs at or just proximal to the patellar inser- tion. Occasionally the rupture may extend into the vastus intermedius tendon or transversely into the retinaculum. Most patellar tendon ruptures occur at the site of origin on the inferior pole of the patella.

Quadriceps tendon rupture > 40 years 

Patellar tendon rupture < 40 years

Risk Factors for Extensor Mechanism Injuries - Chronic systemic conditions, including rheumatoid arthritis, gout, systemic lupus erythematosus, hyperparathyroidism, and iatrogenic immunosuppression in organ transplant recipients, use of steroids/fluoroquinolones. 

Patients with delayed diagnosis of patellar tendon rupture may experience significant retraction of the patella proximally and subsequent development of quadriceps contractures or adhesions. 

Clinical Features. Clinical evaluation can elicit the correct diagnosis in most cases of complete disruption. Classical signs are:
1. Acute onset of pain, swelling, and ecchymoses over the anterior aspect of the knee and a palpable defect in the patella, quadriceps tendon, or patella tendon
2. Loss or limitation of ability for active leg extension - extension lag usually is seen when the last 10 degrees of extension is performed haltingly or with difficulty)
3. High- riding patella (patella alta) with patellar tendon rupture and superior retraction
4. Low-riding patella (patella baja) with quadriceps tendon rupture and inferior retraction. 

Partial disruptions may not show these clinical signs and may require MRI for confirmation.

Diagnostic Imaging
AP and Lateral X Rays Knee

• Obliteration of the quadriceps or patella tendon, a poorly defined suprapatellar or infrapatellar soft tissue mass (represents proximal or distal retraction of the torn tendon), soft tissue calcific densities (represent avulsed bone fragments of the patella or tibial tubercle), or a displaced patella.
• Patella alta may be sought on the lateral radiograph using a ratio of patellar length to patellar tendon length (the Insall-Salvati ratio). The Insall-Salvati ratio (TL/PL) is considered normal between 0.8 and 1.2. Patella baja: <0.8, patella alta: >1.2. 

Ultrasound has low sensitivity and specificity in diagnosing acute quadriceps and patellar tendon ruptures. MRI shows the entire extensor mechanism and is the best imaging modality for diagnosing pathology in this system, even in the acute phase. MRI usually is reserved for patients with possible incomplete disruption or for those with a complication of intra-articular derangements. 

Management

Early Repair - within 2 to 6 weeks of the initial injury. If the tear is only partial, immobilization with the knee in full extension for 4 to 6 weeks is the treatment of choice. Surgical intervention is required for reattachment of complete tendon ruptures, and repair should be performed as soon as possible. After primary repair, the knee is immobilized in full extension with a long leg cast until healing is complete. Gradually progressive active and passive range-of-motion exercises are indicated for optimal results.

Posted by:

              

     Lakshay Chanana

     

     ST4 Trainee

     Royal Infirmary of Edinburgh

     Department of Emergency Medicine

     Edinburgh

     Scotland

     @EMDidactic

Dissociative Seizures

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

Cellulitis Mimics

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

  
  

  
  

Proximal Femur fractures

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

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