Saturday, August 31, 2019

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


Tuesday, July 30, 2019

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. 

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


Sunday, June 30, 2019

Dissociative Seizures

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

Posted by:

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


Saturday, May 25, 2019

Cellulitis Mimics

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)

  • 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 

  • 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